Epidemic Fear

“How many valiant men, how many fair ladies, breakfast with their kinfolk and the same night supped with their ancestors in the next world! The condition of the people was pitiable to behold. They sickened by the thousands daily, and died unattended and without help. Many died in the open street, others dying in their houses, made it known by the stench of their rotting bodies. Consecrated churchyards did not suffice for the burial of the vast multitude of bodies, which were heaped by the hundreds in vast trenches, like goods in a ships hold and covered with a little earth.” -Giovanni Boccaccio, 1313-1375

Conjuring up fear about epidemic infectious illnesses is easy. First bring up the black death that swept the European continent in the middle ages. A little bug wiped out half the population. Fast forward to the Spanish Flu of the early twentieth century. That one was a bird flu that made the jump to humans. Then dip into the African continent where the fiendish Ebola virus rises up periodically and passes easily among villagers, killing virtually everyone infected. And finally move onto SARS, other corona viruses, mad cow disease, AIDS, and flesh-eating bacterial infections. The complacency of the last seven decades of antibiotic and immunization successes succumbs easily to visions of new horrors, which happen to sell well in the crisis-oriented media.

The trick to dealing with the fear of epidemic illnesses is to separate substantiated facts from breathless commentary, identify things within the sphere of your influence, learn what you can and cannot do about them, do those things and quit worrying about the rest. Worry, after all, undermines the immune system, which is the first line of defense against infections of all kinds.

Many of the infectious horrors trumpeted in the press are, for the time being, hypothetical worries that depend on things that might happen, but have not yet and may not ever. That is not to say that our leaders shouldn’t have plans for an epidemic requiring difficult decisions about allocation of resources or for immunizing large numbers of people as fast as possible. But for the average individual trying to lead as healthy and happy a life possible, attention has to go to the “worth-worrying-about category,” – bacteria and viruses likely to be encountered and about which there are things to do to diminish the risk of allowing them to set up shop in the body.

Examples of the “worth-worrying about” category

Three examples of organisms in this category are two different bacteria, MERSA (methicillin resistant Staphylococcus aureus) and clostridium difficile, and the “flu” viruses – influenza type, other upper respiratory viruses that travel in the same circles (corona viruses included here). Ironically, the two bacterial enemies have set up shop in our health care facilities, making trips to the hospital risky ventures for reasons more than whatever brings you there in the first place. The SARS virus did most of its interpersonal traveling in health care facilities, and currently the new coronavirus is most lethal in chronic health care facilities. So, barring bad luck, it is also worthwhile keeping yourself healthy enough to stay out of these places.

MERSA in hospitals – invader of wounds

MERSA first appeared in 1961, two years after the introduction of methicillin, an antibiotic designed to counter bacteria which had become resistant to penicillin. Because bacteria reproduce by the billions, the lucky few that are naturally resistant to antibiotics like penicillin generate millions of equally resistant offspring like themselves in short order. Nevertheless, it took many more years of widespread antibiotic use to spread the methicillin resistant strains around the world. Now they are well entrenched, and account for 40% pf the hospital acquired infections. They travel around the hospitals and nursing homes on the hands and in the noses of health care workers, 40% of whom are “carriers,” and they live on the surfaces of blood pressure cuffs and computer keyboards, waiting to hitch a ride on a hand. Good hand-washing practices are very effective in reducing infection rates, but compliance is surprisingly difficult to achieve. Hospitals in England are contemplating re-instituting the practice of having a matron on each ward to oversee the hygiene practices of doctors, nurses, technicians and patients.

MERSA in the community – boils and other skin infections

MERSA has appeared in the community as well, and it is becoming difficult to tell which bacterial strains originated in hospitals. Typically, the infections caused by MERSA in the community are skin abscesses and inflammation around hair follicles. They afflict people who live in close quarters or share dressing. Prisons, barracks, locker rooms, and communal bathing facilities have all been implicated. While the scary stories told about MERSA have involved rapid deterioration from a quick spread of bacteria along the lines of the connective tissue in an extremity (necrotizing fasciitis), or in the lungs, these cases are rare. The development of a pus-containing, red lump on the skin, around a hair follicle or not, is the most likely presentation, and often can be cleared by a surgical drainage of the abscess.

What can you do to avoid this bug? Take care of any skin breaks promptly, by cleaning them with soap and water and peroxide, and covering them until they are sealed over. Regular baths or showers with good attention to the hair covered areas not only keeps the bacteria count down, but makes you aware of any areas of inflammation, especially if you have been in locker rooms. Keeping sports equipment and clothing clean and dry, especially pieces that come into contact with skin. Alcohol based cleaners are the most effective.

Clostridium Difficile – invader of the colon

Another bacteria making the rounds of health care facilities affects the colon and produces a very nasty smelling diarrheal illness that prolongs hospitalizations, or triggers re-hospitalizations when it appears after a patient has been sent home, in addition to spreading outside the health care setting. Clostridium difficile is aptly named because ridding hospitals of it has been difficult. This bacterium is not a stranger to the colon – over 50% of infants carry it without any symptoms. But when a patient has been taking antibiotics for other reasons, the normal bacterial population of the colon suffers and allows Clostridum D. to move in and irritate its lining, producing diarrhea that in turn requires more antibiotics, which will gradually produce more antibiotic resistance. For the time being C.difficile is still responsive to a variety of antibiotics, and to fecal transplants, but before a patient is adequately treated, his illness spreads the organism further and other sick patients are most at risk. As in MERSA infections, excellent hygiene practices are key to not transmitting clostridial infection.

Flu viruses and other colonizers of the airways

Viral “flus” and upper respiratory infections come around each year in different forms, which may or may not be susceptible to the current vaccines. Vaccines are best guesses as to the from the flu virus will take for the year. Immunization helps protect some people, and is generally recommended for the elderly, the very young and the chronically ill. Because the flu is spread through respiratory droplets, the actions required to minimize the spread of any particularly virulent strain of viruses – the kind that caused the Spanish flu, for instance – depend on an educated and responsible public. Staying out of crowded places, keeping hands away from mouths and noses, adhering to rigorous hand-washing with soap and water before meals and after contact with others, covering mouths with the crook of the elbow when coughing and sneezing, careful washing of food, utensils, countertops, and door handles and use of face masks in public by sick people are all effective ways of curtailing the spread of all respiratory illnesses including the common cold.

Public Defense

The more the public becomes practiced in good hygiene and avoids unnecessary antibiotic use (viruses do not respond to or require antibiotic treatment), the more robust a community’s response to the inevitable breakout of a viral infection will be and the better chance we have of not increasing the numbers of our antibiotic resistant bacterial enemies. Good hygiene also includes maintenance of good general health habits – diet, sleep, and exercise – to keep the immune system primed to ward off invaders and keep individuals out of the chronically ill groups that are susceptible to epidemics when they hit.

You cannot cram for good health but you can keep chronic health problems at bay with slow, steady discipline, a worthwhile endeavor since infections are always worse when other health problems such as diabetes complicate them. Your immune system functions best when you are rested, unstressed, well- nourished, and well-exercised, and exposed regularly to the natural world and sunshine (better than Vitamin D supplements). All of these things are within your sphere of influence and good antidotes to epidemic fear.

Posted by medical plaintalk

Physician turned medical writer.

What is Blood Pressure?

Blood pressure is like the water pressure in your house. The major difference is that spigots in the house open the water to runoff. Unless you start bleeding, your plumbing is a closed system under constant pressure, with a pump at the center that keeps the blood moving through the pipes. The heart pumps blood into the aorta producing systolic pressure, the top number in your blood pressure measurement. This force pushes the blood through a progressively branching network of thick-walled, elastic arteries throughout the body – the arterial side of the circulatory ystem. The branches get smaller and smaller and beyond the smallest arteries, called arterioles, the pressure wave dissipates as the blood flows into a vast network of tiny, thin-walled capillaries, with diameters so small that microscopic red blood cells line up in single file to get through. Press hard on one of your fingertips, enough to make the skin pale, and then let up and watch it grow pink again. You are watching a capillary network fill.

In this capillary network, where pressure in the closed system is the lowest, all your cells exchange their waste products for fresh supplies of nutrients and oxygen. From capillaries, blood flows under low pressure into thin-walled veins and back to the heart. This is the venous side the circulatory system. Between heart beats, a time called diastole when the heart rests and blood pours into it from the venous system, the pressure in the arterial side of the system is at its lowest. This diastolic pressure in the arterial system is the bottom number in your blood pressure measurement.

A house’s pipes are fixed in size and shape. The body’s plumbing is more sophisticated. The muscular walls of the arteries respond to signals from hormones and nerves, with dilatation and constriction necessary to shunt blood to locations where it is needed. When you have a full stomach, your limb muscles give up some of their blood supply (hence the old adage about not swimming right after eating). A good scare reverses this pattern, leaving the stomach queasy and preparing the muscles to fight or flee. In cold environments, blood is shunted to vital organs in the head and torso at the expense of the skin and extremities – the reason that wearing a hat will keep your fingers warmer.

Blood pressure is thus a constantly changing measure of the force of blood flow within the arteries. It goes up with physical activity and comes down with rest. High or low, the pressure is a complex response to the demands placed on the body by activities, emotions, and environment. It is influenced by nutrition and hydration and other health factors. Genetic makeup, as always, plays a role and steers many people toward high blood pressure or hypertension, as they age.

In a small number of cases, hypertension is secondary – a response to an underlying problem (adrenal gland tumor, congenital abnormality of the aorta, narrowing of a renal artery, or genetic endocrine gland problem). In 95% of cases, hypertension is essential – a response to multiple factors that have in common an ability to increase resistance in the smallest arterioles, which forces the heart to pump blood under higher pressure.

Essential hypertension affects an estimated 70 million Americans. Repeated resting blood pressure measurements, over 140/90, without any evidence for an unusual cause, put a patient in this category (more recently some experts are recommending that the number be 130/80, but there is controversy over the subject). Over many years, blood pressures consistently above 140/90 cause slow “end-organ” damage – kidney failure, strokes, hardening of the arteries, retinal damage, and heart failure. The higher the blood pressure, the more the arteries thicken and harden, and the harder the heart has to pump to keep the blood flowing. The more the blood vessels change, the more likely they are to block blood flow, or to rupture, like corroded pipes in a house. And the more rigid they become, the worse the blood pressure gets, especially the systolic component.

How do you know if you have high blood pressure? Symptoms are rare until end organ damage is well underway, so you must depend on routine measurements, and sort out whether or not the anxiety produced by the measuring process is a culprit in raising the pressure. This sometimes means getting a home measuring device, or at least getting repeated checks in an environment away from a doctor’s office. Severe hypertension, with diastolic pressures of 140 or more, can produce headaches, dizziness and blurred vision and is a medical emergency – fortunately uncommon.

Of the numerous factors correlated with essential hypertension, age and family history are the most common and the least “treatable.” But the other common factors – inactivity, obesity, excessive salt intake (greater than 5.8 gms/day), lack of sleep, and excessive alcohol intake – help time accomplish its negative work. These factors, at least, are under some voluntary control, and the platform of treatment of essential hypertension is diet and exercise. For every 25 lbs of weight lost, blood pressure can drop about 3 points. Regular, vigorous aerobic exercise stimulates capillary expansion to accommodate the demand for blood by the nervous system and muscles. Thirty to 45 minutes of daily aerobic exercise yields drops of 5-15 mm, and helps normalize weight. Removing the salt shaker from the kitchen and minimizing processed food drops daily salt intake.

Even with the best of lifestyles, anti-hypertensive medicines are sometimes necessary. Each patient’s health picture determines the best options among the many available drugs. The mainstays of treatment affect the kidney hormones renin and angiotensin (ACE inhibitors), or block the effects of the autonomic nervous system (beta blockers), or help the kidneys release more salt (diuretics). Very often, combinations of two or even three drugs work better than one alone.

Because hypertension produces no symptoms, and its consequences lie far off in the imagined future, sticking with a treatment plan is often difficult. Achieving diet, weight and exercise goals and finding the best drug regimen with the most tolerable side effects require education, patience and commitment, without any obvious rewards (beyond seeing a lower number on the blood pressure monitor) – just like many of the most worthwhile things in life.

What about Meditation?

People skilled in meditation can certainly lower their blood pressure at the time they are practicing the discipline, but blood pressure returns to baseline when they return to routine activity. If the practice of meditation encourages mindfulness in other areas of life it may well decrease anxiety, reduce tension, and improve the self-discipline necessary for dietary restraint, regular exercise, and sufficient sleep – indirectly helping with blood pressure control.

Posted by medical plaintalk

Physician turned medical writer.

Ketosis v.s. Ketoacidosis: Insulin makes the Difference

Ketosis is a word which you may have seen recently in print and online media, usually in material about a very low carbohydrate diet in which most calories come from fat and protein. One recent headline alluded to a plan by the Pentagon to increase military fitness by imposing the “keto diet” on some of its soldiers. But you might also have the impression that there is some controversy around the diet, and that ketosis, whatever it is, might not be good for you. After all, it is very similar to that word ketoacidosis which is associated with poorly controlled diabetes, the problem that put your friend’s daughter in the hospital ICU for a week. In fact, both ketosis and ketoacidosis refer to physiologic body states that occur when come chemicals called ketones are produced from normal metabolic processes that produce energy from the body’s own fat. The circumstances surrounding ketone production determine whether ketones cause ketoacidosis (bad) or ketosis (not so bad but maybe not so good over a long period of time).

How your body produces energy

Most of the time you are utilizing at least some fat to create energy and producing ketones in small amounts as the fats are metabolized. At the same time, the bulk of your energy is derived from the carbohydrates you eat, all of which, even the “healthy” grains, vegetables and fruits, become a simple sugar called glucose in the process of digestion. That is correct – for the most part, you burn sugar to produce energy. Under normal circumstances, with sufficient food and regular eating schedules, some glucose is burned immediately by all parts of the body for energy production. Any remaining glucose gets shuttled off to the liver and muscles to be clumped into long chains called glycogen and stored for use between meals. These reserves last for about 24 hours at which point your metabolism switches over to fat burning, and to breaking down a little protein, mainly from muscle, to supply the liver with building blocks for making more glucose.

The brain has special needs

At this point, you must eat again or rely on free fatty acids from the triglycerides stored in your body fat. The brain, however cannot burn free fatty acids. But it can burn some of the ketones, called ketone bodies, that come from the breakdown of triglycerides. By about three days of starvation, the brain is a ketone burning organ, supplemented by a little glucose constructed in the liver from amino acids given up by proteins. The body is in a state of ketosis, with excess ketones exhaled, giving the breath a fruity odor, and released in the urine, turning a dipstick stick test positive.

Acidity makes the difference

Ketosis is not ketoacidosis. Ketoacidosis appears when the acidity rises in all the body’s tissues while it is in a state of ketosis. Acidity is measured as pH, and a fall in the body’s pH signals rising acidity. Outside a narrow range of pH, the body’s metabolic workings begin to fail. Rising acidity produces symptoms like rapid breathing, nausea, vomiting, abdominal pain, low blood pressure, mental impairment, lethargy, heart arrhythmias and ultimately, if uncorrected, death. In otherwise healthy people, diets that promote ketosis by restricting carbohydrates do not appreciably change the body’s pH, despite the acid nature of ketones and other breakdown products of triglycerides. What keeps severe acidity and its dire consequences at bay? In short, insulin, the central hormone of metabolism.

Insulin keeps the brakes on fat burning

Insulin is secreted by the pancreas in response to eating carbohydrates. In fact insulin is such a reponsive hormone that a burst appears from the pancreas in response to anything sweet in the mouth (the so called cephalic insulin response that prepares the gut to receive expected incoming carbohydrate, even when the sweetness is artificial and no carbs arrive in the stomach). In addition to its role escorting glucose into cells for energy production, insulin keeps the brakes on fat burning. When insulin circulates at normal or high levels in response to carbohydrate ingestion, triglycerides remain locked in fat cells, unavailable for energy production. As night falls and eating ceases, the liver and muscles break down their glycogen to glucose to keep the supply up. When this supply dwindles, insulin levels fall, unleashing fat burning. Free fatty acids and ketones appear in the blood, but in a controlled manner, unless insulin disappears altogether. Then the brakes come off fat burning, fatty acids and ketones flood the system, and their acidity begins to drop the body’s pH.

Ketoacidosis comes from insulin’s diappearance in type 1 diabetes

Type 1 diabetics are the most at risk for ketoacidosis because immune attacks against the insulin producing cells in their pancreases severely diminish or obliterate insulin production. Their blood sugar levels rise because sugar cannot get into cells. Fat burning comes to the rescue for energy production, and, with little or no interference from insulin, free fatty acids and ketones pour out into the blood. In new Type 1 diabetics, before treatment with insulin, major weight loss is very common – as is presentation to an emergency room in a state of profound ketoacidosis, requiring intensive medical care. Once patients are stabilized, urinary ketones are a useful guide for adjusting insulin dose– their appearance means more insulin is needed.

Type 2 diabetes is a different problem

Type 2 diabetics have a different problem, called insulin resistance. Their cells do not allow insulin to bring glucose in from the blood. In an attempt to compensate, their pancreases make more insulin. Blood glucose levels rise, but at the same time high levels of insulin block fat breakdown, preventing the release of large amounts of potentially acidifying fuels, and diminishing the risk of ketoacidosis. But if a crisis such as trauma, infection, or surgery occurs, sugar levels can rise to extraordinary levels in Type 2 diabetics, causing huge amounts of water to be lost in urination as the body passes the sugar out through the kidneys. Severe dehydration and electrolyte abnormalities make this condition, called hyperosmolar hyperglycemia, a crisis requiring intensive care, even without acidosis. When insulin production begins to fail in Type 2 diabetics, ketoacidosis does occur and type 2 diabetics account for 20-30% of ketoacidosis cases in hospitals. One class of Type 2 diabetes drugs, the SGLT2 inhibitors known as gliflozins, has been reported to trigger ketoacidosis.

The caveat about ketosis as a dietary strategy

There is some concern, from epidemiological research, that when a very low carbohydrate diet is continued over the long term, chronic ketosis may trigger insulin resistance, the underlying problem in type 2 diabetes. Insulin resistance is not well understood, but it is associated with a cascade of health problems associated with metabolic problems. If chronic ketosis does somehow trigger insulin resistance, the enthusiasm for deliberately inducing ketosis to lose weight and improve fitness will wane. The word ketosis will fade back into the scientific world.

Posted by medical plaintalk

Physician turned medical writer.

The Life of a Kidney Stone

Under the right conditions, water and minerals combine to create crystals and stones. Towering stone formations called stalactites and stalagmites grow in caves where water drips though mineral-laden rock roofs. In the human body, crystals and stones can form in urine, which is a combination of water, minerals and other waste products filtered out of the blood by the kidneys. If the balance between water and mineral concentrations in the urine tips in the wrong direction, or if the urine becomes too acidic, crystals may form from minerals and coalesce into kidney stones. The physical consequences depend on the size and location of the stones.

Location matters

Stones can form anywhere in the kidney’s “collecting system,” which begins with the calyx, a hollow chamber emerging from the middle of the organ. Urine made by each of your two kidneys fills its calyx and then passes into a long, narrow tube called the ureter. Each ureter connects its kidney high in the back of the abdomen, one on the right side of the spine and the other on the left, to the bladder located , deep in the center of the pelvis below. The bladder is a reservoir where urine is stored until it is released from the body. Symptoms of kidney stones depend on their size and location in the collecting system and on the presence or absence of other problems such as infection.

When confined to the kidney’s calyx, the most common stones, made of calcium, are small and cause no symptoms. But the calyx is also the site where large, branched stones called staghorn calculi can grow and fill the hollow structure, clinging to the kidney tissue and damaging it even to the point of kidney failure. Staghorn calculi are associated with recurrent urinary tract infections caused by bacteria that that cause precipitation of magnesium along with calcium. Staghorn stones are often found as a result of the patient developing fever, back pain and cloudy painful urination – all symptoms of kidney infection. These elaborately branched stones may encase bacteria and grow to huge size before producing symptoms such as blood in the urine, unless a small portion breaks off and passes into the ureter.

The worst pain: when a stone stretches the ureter

A kidney stone may pass from the calyx and through the ureter unnoticed, but if it stretches and irritates the narrow tube as it moves along the resulting pain is intense and colicky, waxing and waning in spasms – and often described the worst pain someone has ever experienced. Ureter pain is felt in the back, between the ribcage and pelvis, or sometimes in the groin or in the testicle. Sometimes fever and bloody urine accompany the pain. Once the stone passes out of the ureter to the bladder, pain disappears.

Bladder gravel

In the bladder, the stone may remain or pass out through the urethra with urination, causing pain with or without bleeding. When stones accumulate in the bladder they are something like gravel, irritating the lining and precipitating frequent need to urinate, burning urination, bloody urine and low pelvic pain. They may also lower the threshold for bladder infections as bacteria cling to the stones, triggering more stone formation and more symptoms. In medieval times, when clothing was changed infrequently and bathing was a yearly event, bladder infections and stones were so frequent and caused such miserable symptoms that people called stonecutters traveled England’s countryside and cities, peddling the ability to remove bladder stones via an incision between the rectum and the urethra. There are even reports of people performing the procedure on themselves.

Who gets kidney stones?

Kidney stones are more common in men that women and tend to run in families. Obesity, chronic bladder or kidney infections, inflammatory bowel disease or a history of gastric bypass, surgery, and prior history of stone formation are all risk factors, as are some rare forms of kidney disease and even rarer parathyroid gland tumors. Doctors don’t know exactly why people form stones, but dehydration is almost always a factor in their appearance. When water intake is low the kidney responds by making urine very concentrated and deep yellow. Concentrated urine contributes to the conditions that promote kidney stone formation. Morning urine is much more concentrated than daytime urine because most people do not drink water during the night. Deliberate lack of drinking water during the day in order to avoid the need for bathroom use makes some people such as surgeons and airline pilots particularly prone to kidney stones. People who live in very dry climates or who lose a lot of water through perspiration may have very concentrated urine without realizing that they are chronically dehydrated.

Diet may play a role

Another factor correlated with kidney stone formation is a high protein diet, which increases urine acidity, promoting crystallization of calcium. High salt diets aggravate the tendency to form stones because as the kidney gets rid of excess sodium, it also pulls calcium into the urine. Curiously, while calcium supplement use may produce kidney stones, calcium from food sources does is not a problem. Rarely, uric acid stones occur in people who have the genetic tendency to gout, or who are taking diuretic hormones.

Treatment

Treatment of kidney stones, like their symptoms, depends on stone size and location. Often, a period of pain control and hydration is often enough to get the patient through the acute problem. If not, the stone can be retrieved from the bladder through a cystoscope passed in through the urethra. A ureter can also be dilated through the scope to remove a stone stuck there. Another technique, called lithotripsy, employs ultrasonic waves applied externally to bombard and shatter stones, rendering them small enough to pass out of the body.

Followup

Beyond the acute phase of treatment, patients who have passed stones need evaluation for conditions like gout, urinary tract infection, and problems with calcium metabolism. Analysis of the stone’s composition can help, especially if it is not the common calcium type. Staghorn stones require more aggressive measures, possibly including open surgical removal.

Anyone who has suffered through the life of a kidney stone needs to be vigilant about drinking water, enough to keep urine very light in color at all times. Weight loss if appropriate, decreasing dietary salt and protein from animal sources, and avoiding calcium and Vitamin D supplements are all helpful in prevention of further stones. Sunlight is a safer source of Vitamin D in those at risk for kidney stones.

Posted by medical plaintalk

Physician turned medical writer.

A Slip of Memory: Transient Global Amnesia

Search the internet for drugs that cause memory problems and you will immediately become familiar with a fascinating syndrome called transient global amnesia (TGA). A website at the top of the list of results opens with these words: My personal introduction to the incredible world of transient global amnesia (TGA) occurred six weeks after Lipitor was started during my annual astronaut physical at Johnson Space Center. TGA is not listed as an adverse effect associated with cholesterol lowering drugs, but with 12 million Americans now consuming these products, recognition of this peculiar syndrome by patients and doctors becomes important. Beyond the tightly controlled world of pre-market drug approval studies, unexpected symptoms need to be noted.

Transient global amnesia is a short–lived problem, over in less than 24 hours. It involves all aspects of new memory formation. Nothing gets recorded during the event and the sufferer fails to remember anything from the event after it is over. To appreciate the disconcerting nature of the syndrome, imagine suddenly losing your ability to put any information into your memory. In addition, you lose access to a few hours or days or even years of past memory, but not to information about yourself. You look around but cannot identify why you are where you are. Depending on how much access to the past you’ve lost, your current situation might be totally unknown to you. With great urgency you question the people around you. “What am I doing here?” How did we get here?” What’s going on?” Someone answers and for about 30 seconds you can hold on to the information. But your ability to put that information into memory has gone offline. You forget that you just asked the question. You ask again, and again, and again, with obvious anxiety. All your other mental capacities work. You can speak, read, write – even drive and problem solve. Except for your anxiety, you are the same person as always. Then the confusion ebbs. You start to encode information again. Your past gradually returns, in chronological order. Once again you are tethered to time and place, but you will not ever remember what went on while you were cut loose and for a little while you might complain of a little headache.

The first descriptions of this odd set of symptoms appeared in an obscure medical journal in 1956. More cases came to light, and by the early 1990s there were a few epidemiological studies that suggested that TGA occurs in about 10/100,000 people, or as many as 25-32/100,00 in the peak age group of 50-80. Far from being a harbinger of impending stroke or evidence of seizures, these episodes seemed to have no correlation with any problems other than a history of migraine and left no problems in their wake. They recurred in somewhere between 5 and 25% of the cases, with one patient having over a dozen recurrences. No definite cause has ever been found, though many physicians have associated them with immediately preceding, physically or emotionally strenuous events.

Very rarely, underlying brain problems like tumors involving the deep middle and frontal areas, where memory formation takes place, turn up in TGA cases, but careful examination of these cases inevitably reveals some deviation from the typical clinical symptoms, or some type of abnormality on neurological examination. TGA research studies, using sophisticated scanning and EEG techniques, suggest that there is decreased activity in areas of the brain involved in memory formation, but give no clue about the mechanisms involved.

In 1990, criteria for diagnosis of the syndrome were published (listed below), and when a diagnosis of TGA strictly adheres to these criteria, it is almost always safe to predict that there is no underlying neurologic or vascular problem. Nevertheless, when a patient appears in an emergency room with TGA symptoms, good practice still requires a CT or MRI scan and an EEG at some point to rule out the remote possibility of an underlying tumor, hemorrhage or seizure disorder.

Reports like those of Dr. Duane Graveline, the astronaut/physician author, are considered anecdotal and not of the same value as information gleaned from statistical analysis of controlled studies . The cholesterol lowering drugs are in widespread use and considered very safe by most physicians. However, there have been cases of muscle and nerve problems, as well as cases of decline in cognitive function attributable to the drugs, possibly mediated by damage to mitochondria, the power houses of all cells in the body. Since the drugs are viewed as valuable additions to the battle against heart disease and are likely to be used over long periods by increasing numbers of people, it is important to understand and catalogue their unintended consequences. Once drugs reach large populations outside medical studies, more problems emerge, sometimes beginning as odd, single cases. In the meantime Dr. Graveline has died after a progressive illness which resembled Lou Gehrig’s Disease (progressive loss of muscular strength and bulk). His memory, however, remained good.

Diagnostic Criteria for Transient Global Amnesia

A witness must be present to describe what happened.
The patient must be unable to form new memories of any kind (anterograde amnesia).
The patient must have full knowledge of his identity and an unclouded state of consciousness.
All other mental functions are normal, including speech.
There are no other neurological symptoms or signs.
There are no signs of a seizure.
There is no history of seizures within the last 2 years, or of recent head injury.
The patient is back to normal within 24 hours.

Posted by medical plaintalk

Physician turned medical writer.

Floaters

Eventually, everyone sees floaters- the dark wavy lines or spots or cobwebby filaments that drift lazily through the visual field of one eye or the other. Quick eye movements up, down or sideways will clear them from your line of sight, but slowly, because floaters move through a jelly like substance in the center of the eyeball. Like the ghosts wandering around Harry Potter’s Hogwarts School, ocular floaters are most often harmless annoyances. And like so many of life’s problems, they are an accompaniment of aging, particularly in people who are nearsighted (those who require glasses to see clearly at distances).

Blame aging
Aging produces changes in collagen, the structural protein that gives form to much of the body. As a result, we develop skin wrinkles, stiff tendons, unpliable heart valves and brittle cartilage, to name just a few obvious accompaniments of living to old age. Few people know that there is collagen in the middle of the eye, which is filled with a glob of jelly-like material called the vitreous humor. Most descriptions of the vitreous humor conjure up a picture of a clear, colorless ball of Jell-O that fills the posterior chamber of the eye (the space between the lens behind the pupil and the retina lining the interior of the eyeball). The vitreous keeps the eyeball from collapsing and helps hold the retina in place.

Vitreous humor – a complex structure

But appearances are deceiving. Though the transparent, jelly-like glob is composed of 99% water, it is also a delicately complex structure in which collagen plays an important structural role. Like skin, the vitreous ages. Along with the years come the floaters.
You are born with the vitreous humor in place. Should it be removed, by surgery or trauma, you will not grow another. This is in contrast to the aqueous humor, a clear liquid that fills the space between the cornea that protects the eye and the colored part called the iris (called the anterior chamber of the eye – see diagram). The aqueous humor is manufactured by the ciliary body, a muscular structure that gives rise to the iris. From its manufacture point just behind the iris, the fluid circulates through the pupil, fills the space behind the cornea, and exits via a channel formed by the junction of the iris and the cornea. This evenly balanced system of fluid manufacture, circulation and exit controls the pressure within the whole eye. No such recycling system exists for the vitreous humor – as in Las Vegas, what happens in the vitreous humor stays in the vitreous humor.

What happens without recycling?

The collagen structure within the vitreous humor is an airy honey-comb of interconnected collagen fibrils – microscopic fibers cross-linked and held apart by chemical and electrostatic forces. The network is loosely attached at some points to the retina that lines the inside of the back of the eyeball. The spaces in the honeycomb contain a solution of many minerals and polysaccharide molecules (chains of sugars) dissolved in water. The collagen network is, in part, held open by the pressure of the watery solution. With age, the system has mini-collapses of collagen fibrils, resulting in some clumping of the collagen networks. Floaters are the result. Occasional macrophages (white blood cells that clean up debris) float about, but they are a lonely workforce.

When are floaters more than a nuisance?

A sudden increase in the number of floaters, accompanied by transient light flashes, is sometimes indicative of a segment of the vitreous pulling away from an attachment point on the retina. This condition is known as a posterior vitreous detachment. By itself, a posterior detachment is not a serious problem, but occasionally the point of shrinkage also pulls the retina away from the vascular layer underneath it. Now you have a retinal detachment, and your vision either develops a blind spot or the sensation of a curtain pulled over part of the visual field. Such symptoms require immediate ophthalmologic evaluation and treatment to prevent further detachment of the retina.

Treatment

There is no special treatment for floaters but at times, floaters are troublesome enough for an ophthalmologist to attempt to remove the vitreous humor entirely. The surgery is very difficult and fraught with hazards such as retinal detachment or damage resulting in partial blindness. Called a vitrectomy, it is a procedure done more often for other reasons such as eye trauma. After vitrectomy, the vitreous has to be replaced to maintain the shape of the eye. Research by physicists and bioengineers on suitable replacement substances has been the biggest source of information about the physical nature of the vitreous humor and the origin of the near universal phenomenon of floaters. However, to date the replacement is still done with saline, which is then naturally replaced by the same fluid that fills the anterior chamber.

Natural history of floaters

What happens once you begin to notice floaters? They come and they go – eventually sinking out of view. The process is very slow because there is no circulation pattern in the vitreous humor and the body has not assigned a vigorous cleanup crew to the problem. Because of this slowness, and because the vitreous passively absorbs substances from the bloodstream via the blood vessels in the retinal layer, coroners sometimes use the vitreous humor to search for toxic substances like drugs at autopsy. Chemical traces remain there after they have disappeared from other body fluids; and. the vitreous humor also retains its integrity longer than other parts of the body.

Plato’s cave

As for “seeing” floaters? You are not actually looking at the clumps of collagen. Just as in Plato’s story about people in a cave interpreting shadows created by firelight as reality, you see only the shadows of floaters cast on the retina by light coming through the pupil. For this reason, floaters are clearest when you are looking at a bright background such as snow or water. Even when you see floaters with your eyes closed, light is passing through the thin eyelid and into the pupil, the only opening in an otherwise light proof box. Who knew these little annoyances could illustrate a philosophy lesson?

Posted by medical plaintalk

Physician turned medical writer.

Medicine by the Numbers: Statistics

A good decision is based on knowledge and not on numbers. Plato

Posted by medical plaintalk

Physician turned medical writer.

The Role of Alcohol in Dementia

O God, that men should put an enemy in their mouths to steal away their brains!”

Cassio (Act II, Scene iii) William Shakespeare

The Diagnostic and Statistical Manual of Mental Disorders, the official compendium of acceptable psychiatric diagnoses, lists a syndrome called “alcohol-induced persistent dementia.” This condition was once described as the “common end reaction of all alcoholics who do not recover from their alcoholism or do not die of some accident or intercurrent episode.” But alcoholic dementia has never been a frequent diagnosis and alcohol is still not listed as one of the risk factors for dementia. In guidelines for reduction in harm from alcohol consumption, the governments of the US, Canada, Australia, Great Britain and the EU all acknowledge the role alcohol plays in a host of chronic health and social problems, but dementia is not mentioned. Growing epidemiological evidence suggests that this omission is an error, and even that alcohol-related dementia might be a “21^st-century silent epidemic.”

Epidemiological Evidence

Some evidence comes from a 2018 British study that correlated the appearance of dementia with the alcohol habits of British civil servants over a period of 23 years. The data showed that people consuming more than 14 units of alcohol a week (the equivalent of 60gm of alcohol or about 6 drinks) had an increased risk of developing dementia. The more they consumed, the higher the risk. A 2018 French study concluded, from a vast analysis of hospitalizations related to alcohol disorders, that there was a distinct association of alcohol use disorders with all kinds of dementia, that alcohol was responsible for a much greater proportion of dementia than previously estimated, that alcohol should be considered as one of the main causes of dementia appearing before age 65, and that, of all the risk factors related to dementia, alcohol was the easiest one to change.

A subject that doctors and patients avoid

Abstinence, over time, improves the symptoms of alcohol related dementia. Why, then, do we not make vigorous attempts to educate patients and families in the early stages of dementia evaluations about the possibility that ceasing all alcohol intake might be beneficial, and certainly not harmful, no matter what the cause of the dementia? Doctors who evaluate patients for symptoms of dementia should question patients carefully about their current and past alcohol use patterns. Often, they do not. Patients being evaluated for dementia, and the concerned family members who bring them to the doctor, should provide honest and accurate accounts of alcohol use. Often, they do not. Alcohol use is a subject which people tiptoe around for many different reasons, but one which should be addressed openly and compassionately, with an educational goal.

The path of alcohol through the body

The first goal is understanding how alcohol affects the brain, and how age and sex influence its effects. Alcohol is absorbed into the bloodstream within five minutes of entry to the stomach. On its first pass around the body, it is metabolized by an enzyme called alcohol dehydrogenase. This enzyme declines with age and is less active in women than in men. Alcohol that is not metabolized immediately circulates in the blood and is measurable as a “blood alcohol level.” Some of it goes to the liver where it is broken down to a substance called acetaldehyde and some is broken down to acids – all these chemicals escape in urine, as well as in your breath and through the skin (the source of the “morning after” boozy smell that lingers long after the party is over). In the brain, the un-metabolized alcohol enters brain cell membranes and dissolves some of their fats, changing receptors that transmit information from cell to cell. As more and more alcohol is absorbed, blood alcohol levels rise and a predictable sequence of events occurs: mild euphoria, mild in-coordination, then imbalance, confusion, depressed mental activity, stupor, deep anesthesia, and, ultimately, death.

Tolerance reflects changes in brain cell membranes

Depending on tolerance, alcohol’s effects on brain function occur at varying blood alcohol concentrations, with some alcoholics able to remain awake and alert at blood alcohol levels that might kill novice drinkers. Enzymatic breakdown of alcohol occurs a little faster in people accustomed to heavy drinking, but most of their tolerance to alcohol’s effects comes from persistent changes in their brains.

Altered brain cell membranes change the personality

Brain scans of chronic alcoholics typically show atrophy – shrinkage of the brain tissue, and, at autopsy, the brain of a chronic heavy drinker may show loss of some cells and white matter. But unless there are coexisting problems like old trauma, Alzheimer’s disease or vascular damage, there is no specific pathology that identifies alcoholic dementia. In life though, the result of altering brain cell membranes chronically by dissolving parts of them in alcohol is dementia – the gradual disintegration of a personality structure with persistent impairments in attention and memory, problem solving, language use, planning abilities, visuo-spatial understanding, and in emotional control and responsiveness. Memory problems can be the most prominent feature in alcoholic dementia, and emotional instability and paranoia also occur.

Not all bad

Is all alcohol bad for the brain? Not necessarily. Both studies mentioned earlier confirm a modest increased risk of dementia in strict teetotalers, an observation made many times in the past and never well understood. Research in the last decade suggests that small amounts of alcohol enhance the function of the “glymphatic” system, a term coined to describe the way spinal fluid flows deep into the brain and clears waste from it. Sleep and exercise also heighten this pattern of spinal fluid flow. (Exercise is known to have a protective effect on the brain, lowering dementia risk. Sleep deprivation, at its extreme, produces symptoms indistiguishable from dementia. More research into the glymphatic system may help explain these observations.) The slightly increased risk of dementia in teetotalers is not considered a reason to begin drinking for someone who prefers to abstain.

Understanding alcoholic beverages

Knowledge and awareness are keys to moderation in alcohol consumption. The alcohol in beer and wine comes from fermentation of sugars. Alcohol in whiskey, vodka and other spirits comes from distillation and the process produces additional chemicals which are like alcohol, but more toxic. The percentage of alcohol in beers, wines and spirits can vary widely. As a rough guide, standard drinks like a 12 oz. beer (typically 5% alcohol), a 5 oz. glass of wine (12%alcohol) and a 1.5oz. shot glass of distilled liquor (40% alcohol) contain roughly the same amount of alcohol – 12-14 gms. Label reading is important since the percentage of alcohol can vary significantly among different beers and wines. A 12 oz. craft beer may be the equivalent of 1.4 drinks because of a 7% alcohol content.

The risk of dementia begins to climb after about 60gm/week for men and 40gm/week for women on a regular basis – about 5-6 servings. It takes about an hour to metabolize 150 mgm of alcohol/per kilogram of body weight, which translates to about 1 oz. of 90 proof whiskey for a man of average weight. Take in more over that hour and the excess alcohol circulates in the blood and begins dissolving membranes in the brain, and mental effects appear. As alcohol is cleared from the body recovery occurs in the brain and the mental symptoms resolve. With chronic, repetitive, excessive exposure, some changes fail to reverse and dementia is the result.

If you are concerned about alcohol “stealing away your brain,” and want to rethink drinking, there is much useful information for you at the link below.

https://www.rethinkingdrinking.niaaa.nih.gov/How-much-is-too-much/Whats-the-harm/How-Can-You-Reduce-Your-Risks.aspx

Posted by medical plaintalk

Physician turned medical writer.

The Gratitude Attitude: Five Best Days

Gratitude is an attitude that mental health professionals say promotes mental well-being. They advise practices such as noting three good things about each day and writing them down at night. Studies actually show that such habits durably improve mood. In the giving spirit of the Christmas season I would like to share with you one of our family traditions that, in retrospect, I realize promotes the gratitude attitude over the course of each year.

We began taking our boys to Colorado to learn to ski when they were very little. Economic and time constraints meant one week a year, determined by my husband’s surgical on-call schedule. That week included the turn of the year on New Year’s Eve. Children’s skiing torchlight parades, followed by dinner at a Chinese restaurant and early bedtimes gradually gave way to a movie (usually laughably bad) followed by dinner at a locals’ Italian restaurant with paper-covered tablecloths and crayons for doodling. The family expanded to include our boys’ friends – first as children and teenagers along for a vacation, then as young men who worked as ski instructors. Somewhere along the way we began the habit of discussing our five best days of the year over New Year’s Eve dinner.

The crayons and the paper table covers are very convenient – everyone begins jotting down their five best days, in order, almost as soon as the menus arrive. The entire dinner time winds up devoted to going around the table in five rounds, hearing from each person about what made each wonderful day and how they decided where to rank it in the list. The choices are life stories in snapshots, changing with growth and priorities. They are funny, poignant and surprising. We also hear from people who have been with us on past New Year’s Eves, calling, e-mailing, or texting their top five days, sometimes accompanied by pictures. They all get heard.

The reason this tradition promotes gratitude is a very practical one. If you know you are going to have to come up with your five best days of the year on New Year’s Eve you learn pretty quickly that memories are weak. You cannot cram for this test. You have to start noticing potential top five days as they happen over the course of the year. You start writing them down. Pretty soon you actually have a little journal and it contains good stuff. The good things that happen in life start to break into your awareness and compete with danger-surveillance program that runs continually in the background of your mind. All good, with none of the side effects of mood enhancing drugs (which fail in the long run anyway).

Just as a matter of historical interest, we traced this tradition back to its origins. It actually began with my husband’s surgical training at Massachusetts General Hospital. The surgical interns and residents on the general surgery service met at the end of each day and were asked to talk about the cases they helped with and to explain what they had learned. The practice helped everyone process what they had done and learn from their experiences. As a family, we were always sit-down dinner people, with candles even when there was still a high chair at the table. Like the surgery residents, we always talked about everyone’s day. Skiing days included lots of bests. Best fall, best jump, best run, best lift ride. The evolution to a summing up of bests at the end of a year was inevitable. What is a surprise is the way the practice has continued and spread from our families to others. Maybe you would like to give it a try.

Posted by medical plaintalk

Physician turned medical writer.

Human Diversity: A Mind Thing

(A version of this essay was published in Minnesota Medicine in March, 2005.)

The first snowy egret I ever saw was standing in a shallow pool, a beautiful white creature with a wispy headdress floating in a gentle breeze. When he lifted off, trailing his long black legs, I was startled by a flash of bright yellow – he looked like he was wearing a child’s rubber boots, designed to hug a bird’s clawed feet. He did a loop around the pond in flying low in a peculiar, non-aerodynamic position. His legs hung down rather than stretching out parallel to his body. He dipped closer to the water and his dangling yellow feet brushed the surface. He’s landing, I thought. But he didn’t. He repeated the maneuver four times. He’s afraid to land, I thought. But then he touched down with hardly a splash, and dipped his beak to catch a fish, then another, and another. In a moment of bird-watching epiphany, I realized that his feet were like a fisherman’s lure. He’d rounded up his lunch.

I looked around the pond. I’d just watched a bird with bright yellow feet use them to attract the curiosity of his prey. Across the water was a bird with a lower bill that expanded into a pouch to collect fish as he skimmed, openmouthed, over the water. Perched high above was another, just about to dine on a large fish he’d skewered with fearsome talons. What an impressive display of diversity! If people were this diverse, New England fishermen would grow waterproof, blubber lined hands, typists would develop extra fingers, and mothers really would have eyes in the backs of their heads.

But people are pretty much the same as far as their bodily equipment goes. Five fingers on each of two hands, ten toes divided between two feet, two eyes, upright posture, and a narrow range of physical abilities, notwithstanding the spread between ordinary and Olympian. The traits we associate with human diversity are superficial – hair color and texture, skin color, facial appearance. Almond shaped or round, eyes still see. Long, elegant skeletal frames and short squat ones all support bodies against the universal force of gravity. Skin pigmentation protects the body covering from the sun, more or less depending on the power of the sun in the areas of the world where the people originated. We are much more like each other than we are different in our biology. The birds have it all over us in the diversity contest.

After my egret experience, I packed up my binoculars, got on my bike and headed home, humbled a little by the thought that all of the talk and concern about diversity among people is overblown, maybe just another representation of man’s abiding sense of self-importance. But along the way I passed bikes and cars, houses and stores, a radio broadcast tower, and a museum. I crossed a bridge between two islands and waved to a fisherman in his boat. And I realized that each of these man made things I passed began as an idea, somewhere, some time, in somebody’s head. We might not differ much in anatomy and physiology, but no two of us have identical thoughts. The mind is the site of the real diversity among humans. The mind is plastic and ever developing. It records, collates, recalls, communicates, and combines unrelated information in new ways. Yellow feet catch the eye, but minds change the world.

Posted by medical plaintalk

Physician turned medical writer.

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