Chilly Treatment

Large scale studies of survival after cardiac arrest have produced dismal statistics, with survival to hospital discharge of 17.6% when the patient is already in the hospital at the time of the arrest and only 6.1% when the arrest occurs outside the hospital.  The development and widespread deployment of portable automatic external defibrillators (AEDS) in public places has increased the number of people who make it to the hospital after cardiac arrest.  However, the survivor’s longer term outcome depends in large part on how much brain damage occurs during the arrest and whether or not the restoration of circulation damages the brain further, a phenomenon called reperfusion injury.  Because the odds of initial survival have improved, and because lowering the core temperature of the body appears to lessen reperfusion injury, the subject of hypothermia has emerged as a vibrant area of research and therapeutics.

Therapeutic hypothermia is an old idea

Hippocrates (460-370B.C.) recognized the value of cold temperatures in the outcome of soldiers with head injuries and in people suffering from tetanus. In the 1800s, Napoleon’s surgeon used ice to prepare limbs for amputation because it numbed pain and reduced bleeding. Over much of history, miraculous recoveries were reported in victims of cold water submersion. But not until the late 1950s did therapeutic hypothermia become a routine part of some surgical care, when experiments in animals demonstrated its value in protecting the brain during the open-heart surgery.  Despite some attempts to cool patients for other problems such as cardiac arrest, strokes and head injuries, the number of problems encountered in during cooling and in the re-warming phase put a damper on the use of the technique. Now, however, we are in the middle of a revival of interest in therapeutic hypothermia.

How does cold help?

Cold protects the brain because the biochemical reactions that sustain life are influenced by temperature. If the heart stops, the brain runs out of fresh supplies for energy production in two minutes. A downward spiral toward brain cell death begins unless blood flow is restored within the next two minutes. When blood flow is restored (reperfusion), a cascade of potentially damaging chemical reactions begins in cells that have been deprived of oxygen. The longer the period of arrested circulation was, the more damaging these reactions are.

The body at different temperatures

Changing the body’s temperature changes the speed and efficiency of its chemical reactions.  At temperatures over 105 many processes fail completely. As body temperature falls below normal, chemical reactions slow down.  Between 92 and 89.6  the damaging chemical responses that come after blood flow returns are blunted enough to improve outcomes significantly.  By 90, pulse and respirations slow and peripheral circulation shuts down. By 86 the patient may still be alive, but looks dead. This level of deep hypothermia is used for some long, difficult cardiac and neurosurgical procedures.

Lowering temperature is now routine, sometimes

Since 2005, the American Heart Association has recommended therapeutic hypothermia as a routine part of patient care after a cardiac arrest in circumstances that depend on the reason for the cardiac arrest, the speed of the resuscitation, and the state of the patient after circulation is restored.  Some medical centers are also experimenting with the technique in the treatment of certain types of strokes and head injuries.

How do you lower someone’s core temperature?

How do you cool a body that normally maintains a constant temperature that hovers within a few tenths of a degree of 98.6?  Any environment with a temperature less than body temperature provides a gradient for heat loss.  Deliberately making someone hypothermic means increasing that temperature gradient. In the presence of a gradient, heat radiates away from the body. Heat is also conducted away when the body is in contact with any colder substance; when the colder substance such as air or water is in motion, heat is lost even faster, by convection.  Heat is also drawn away by evaporation of perspiration on the skin’s surface, where the sweat keeps the microclimate humidity at 70% even when you think you are dry.   Heat also dissipates when warm moist air is exhaled from the lungs.

Several internal and external ways of changing the temperature gradient  exist: ice packs applied to the head, neck, axillae, groin, where large blood vessels are close to the surface; cooling blankets that house cold water circuits; closed catheters through which cold saline circulates inserted into large blood vessels; ice water balloons in the bladder.    These methods are directed at the core temperature of the body – the temperature of the internal organs and the brain. They do not cause problems like frostbite, seen commonly with accidental hypothermia, because the ambient temperature is not freezing and the skin is protected from direct exposure to ice packs being used for cooling.

The body resists lowering the temperature

Normally, we protect ourselves from falling temperatures by putting on more clothes and increasing activity, and by shaking and shivering, which produce heat.  A patient who has suffered a cardiac arrest will not engage in the normal behavioral responses, but he will shiver and perhaps become agitated, both of which are counterproductive to getting the temperature down. Sedation and even muscle paralysis are therefore necessary for the period of cooling.

Despite problems,  therapeutic hypothermia is here to stay

Current therapeutic hypothermia protocols call for maintenance of temperature between 32-34 (89.6-93.2) for 18-24 hours, followed by passive re-warming over the next 24 hours. Overshooting and undershooting of temperature are both common, as are difficulties maintaining electrolyte and sugar balance. Some complications like pneumonia and bleeding problems are more common than in similar patients not being treated with cold temperatures. Much work remains to determine the best timing for induction and maintenance of hypothermia after cardiac arrest, but it is clear that “the sooner the better” is the general rule and that the revival of interest in therapeutic hypothermia is here to stay.

The Latest on Charley Horse: How Muscle Cramps Work

No one knows for certain how “charley horse” became a name for muscle cramps.  Baseball lore from the late 1800s links the term to a player named Joe Quest, who may or may not have compared his cramp-prone teammates to an old, stiff-legged white horse named Charley who pulled heavy loads in his father’s machine shop in New Castle PA. The first newspaper story using the term charley horse in the context of players who pulled up with thigh cramps was allegedly the Chicago Tribune, during Quest’s 1879-1882 stint with the Chicago White Stockings. The first retrievable story using the term, in the Boston Globe in 1886, referred to the Tribune story as the origin of the name. By that time, Quest was with the Philadelphia Athletics and at the end of his career, but the off-hand description he may or may not have coined has become a household word, spread far beyond the world of baseball.

What is a muscle cramp?

Muscle cramps of are involuntary, intense and painful contractions which harden the muscle and last seconds to minutes. Aching pain and even chemical indications of muscle damage may persist much longer.  Electrical recording of muscle activity during cramping and between bouts of cramping indicates that the baseline or normal amount of electrical activation of the muscle is increased – maybe a measurable correlate of the feeling that a muscle is “about to cramp.”

Theories about cramps

Long-held theories have blamed muscle cramps on dehydration, electrolyte losses from sweating, extreme environmental conditions of heat and cold, or inherited problems of energy production. In addition, cramps happen more in people taking some medications some medications such as cholesterol lowering drugs and diuretics. While these factors may play supporting roles, they do not explain the mechanism of cramping. Nor do they explain why stretching, as well as folklore-based remedies like the Amish combination of vinegar, ginger and garlic, or consumption of pickle juice, mustard or hot peppers help cramps. Newer, “neural” theories about the mechanism of cramping, which implicate feedback loops between muscle and the spinal cord, might account not only for exercise related cramps but also for and the kind that grab hold of a leg as you roll over in bed.  And they might explain the seeming success of peculiar remedies. To understand the neuromuscular feedback loops we must diverge briefly into a little muscle anatomy and physiology.

How your muscles move things

When you decide to lift this magazine, your brain sends a message to motor nerve cells in the spinal cord, the alpha motor neurons, which then fire signals down nerves to the biceps muscle and to all the other muscles are involved in the task, telling some to contract and others to relax.   That is the simple part. The complex part, which goes on in the background at all times, is the feedback from two types of specialized muscle receptors which act much like strain gauges used in civil engineering to detect forces deforming land and buildings.

Strain gauges in every muscle: moderators of muscle tone

One type of muscle receptor strain guage is a muscle spindle. It calculates stretching forces in the belly of a muscle. The other is a Golgi tendon organ, which calculates the stretch in the tendon, the fibrous end of the muscle that attaches to bone.  Muscle spindles send messages to the spinal cord motor cells to fire up and contract the muscle when the muscle lengthens too much. Golgi organs send the opposite message to prevent the tendon from becoming too tight as the muscle contracts. All of this occurs rapidly and constantly, in a balance that keeps your muscles at the right degree of tone for all your movements.

In 1997, researchers suggested that unbalanced feedback from these little muscle strain gauges was the primary cause of cramping.  In fatigued muscle, at least in animal studies, the spindles were more active than normal, and the Golgi tendons less active.  The net result caused alpha motor neurons to fire up the muscle fibers than they usually do. Passive stretching of the muscles, which stretches tendons, woke the Golgi receptors back up, prompting them to send more cease and desist orders to the motor neurons. The cause of cramping thus appeared to be too much spindle input.

Regulation from above

Motor neuron feedback loops also receive input via pathways that originate higher in the nervous system. Swallowing liquids with striking tastes stimulates sensory cells in these spinal pathways, sending messages up to the brain and down through the spinal cord. Cramp researchers speculate that stimulation of these pathways tamps down some of the incoming messages from the muscle spindles, providing an explanation for the efficacy of some old-fashioned cramp remedies.

The well-known tendency of baseball players to suffer cramps might also bolster the neuromuscular feedback theory.  Baseball players wait to explode into motion from crouches, get up from slides to race back to safety after failed base stealing attempts, and stop, start and reverse direction abruptly.  It is easy to imagine some Golgi tendon organs and muscle spindles lulled into altering their feedback and then lagging in adjusting to the abrupt new actions.

Cramps in bed

But what about the cramps that are not associated with the fatigue of exercise? Shortening of the muscle in certain positions, such as lying in bed, may set them up for the same imbalance in input from the stretch receptors. The increasing frequency of cramp problems with age could be a result of general loss of strength and flexibility in muscles that are not used as much as in the past.  The ideal input from muscle stretch receptors occurs in the rested muscle which has maintained its youthful length and flexibility.

Practical application of the latest theory

Practical application of the neuromuscular feedback theory of cramping applies not only to charley horses, but also to musculoskeletal injury prevention in general.  Maintenance of flexibility and balance of strength in opposing muscle groups such as the quadriceps and the hamstrings keeps the spindles and Golgi tendon organs in balance, and muscles which are less stiff and prone to cramping allow movement with less discomfort as life moves on. Such maintenance requires regular work, especially if you want to avoid some of the creeping stiffness of old age.

Note: the muscle receptors and their connections  may well play roles or even be the culprits in some mysterious muscle disorders that are associated with cramping or decreased muscle tone. Muscle research is a blossoming field in this new age of genetic research. All muscles bear the stamp of their genetic makeup in their differing structural proteins. Some people have big bulky muscles, some long slender ones; some have more fast twitch fibers that make them speedy, others more slow twitch fibers that endure for marathons.  And some people are relatively inflexible, others loose and prone to twisting ankles. You get what you get from the usual complement of both parental versions of DNA, in the nucleus of the cells. (But if you want to complain about your speed, blame your mother- she provided all the DNA in the mitochondria which power the cells.)

Tetanus: Poster Child for Preventive Medicine

 

True preventive medicine is an intervention that stops a disease from developing, not one which simply slows disease progress. The body’s immune system is the master of disease prevention and it is no accident that one of the first medical efforts at preventing disease stemmed from the observation in the late 1700s that suffering a mild infection like cowpox prevented a similar but more severe infection – smallpox. Immunization was born, and to this date is the single most effective form of prevention of lethal disease. In the current age of rejection of routine immunization by a significant number of people, the disease called tetanus and its prevention by immunization is a story worth reviewing.

What causes tetanus?

Tetanus a disease is caused by a type of bacteria called Clostridia tetani, a fragile little organism that can’t tolerate oxygen or high temperatures but which changes itself into a tough intermediate form called a spore to lie in wait for potential victims. C. tetani spores survive indefinitely, are common in soil, particularly manure rich soil, and are found in intestinal tracts of farm animal, cats, guinea pigs, rats and people. They can survive oxygen rich environments, the usual antiseptics and even the temperatures used to sterilize medical instruments. Once the spores gain entry into body tissues, they revert to fragile bacterial form, reproduce and begin to manufacture tetanospasmin, one of the most lethal toxins known to man and the substance responsible for the symptoms of the disease. Though farm animals and people are susceptible to tetanus infection, dogs and cats are not.

Development of symptoms

Tetanus infections are usually acquired when C. tetani spores enter the body through a deep wound in the skin that air does not reach. Contaminated batches of heroin are also sources of infection when the drug is injected under the skin or intravenously. In the first few days after C. tetani spores come to life inside the body, no symptoms or tests indicate anything amiss. As the toxin producing bacteria increase in number, and the toxin produced finds its way to the spaces between nerves and muscle and between motor nerve cells in the brain and spinal cord, profound muscle spasms begin. Tetanospasmin works by the blocking normal neurochemical signals that inhibit muscle tone and motor nerve excitability.
The time from infection to development of symptoms in any infection is known as the incubation period. In human tetanus, the closer the entrance point of the bacteria to the brain or spinal cord the shorter the incubation period. On average symptoms begin about a week after injury. Though localized forms of tetanus can occur, with muscle spasm limited to the area around the wound, most cases are general and symptoms begin in the muscles of the head and neck. Spasm of the powerful masseter muscles of the jaw is the origin of the term “lockjaw,” a commonly used name for tetanus infection. Vocal cord and respiratory muscle involvement can interfere with breathing. Abdominal, trunk and skeletal muscle involvement are extremely painful and spasms can be strong enough to fracture long bones and spinal vertebrae. Other complications arise from involvement of the central nervous system: fever, high blood pressure, heart rhythm abnormalities and seizures. Secondary complications like bladder infections, pneumonia and blood clots in the legs and lungs also contribute to the lethality of the disease. In the pre-immunization era, treatment was confined to supporting the patient through the four weeks it takes for the toxin’s effects to wane.

Making the immune system remember the disease

Unlike cow pox, in which the natural immune response directed against the cowpox virus prevents more cowpox episodes but also smallpox, a full-blown case of tetanus does not confer any immunity because the minute amounts of toxin that produce the symptoms are not sufficient to stimulate the immune system to make antibodies against it. Immunization to tetanus is accomplished by presenting the immune system with a much larger amount of a formaldehyde weakened version of the toxin, to which it will produce antibodies which will neutralize the real toxin should it ever appear. This process takes a few weeks and several doses are required over time to reach full potency of an antibody response.

Immunization programs have made tetanus rare enough for people to forget how terrible an illness it is. In the US, since routine, active immunization began in the 1940s, tetanus rates declined steadily and were at an all-time low of .01 cases per 100,000 people in 2009. In addition, with better supportive care, mortality rates declined from 30% in the mid-1900s to 10% in the first decade of the 21st C.

Borrowing someone else’s immunity

Nevertheless, tetanus infections still occur and may increase in frequency if immunization rates drop. Fortunately, another type of immunization helps when tetanus develops in people who have not been immunized – a passive immunization process that allows patients to borrow antibodies produced in the blood of other people who have been immunized against C.tetani. This “antitoxin” is a mixture of human gamma globulin from screened donors and antibodies in it that “recognize” tetanus toxin react with the toxin circulating in the tetanus victim’s body, neutralizing a lot of its potency.

Boosting weakened immunity

The antibody response to tetanus toxoid wanes over time, but a repeat injection brings it up to full speed quickly. Booster doses are recommended for all adults every 10 years and in the event of penetrating wounds, especially if immunization status is unknown. Awareness of the symptoms of tetanus and the status of immunization of anyone someone suffering from heroin addiction, a sad and growing problem, is crucial for anyone who cares for them. Tetanus is the poster child for preventive medicine and no one should have to suffer this disease. The earlier it is recognized, the better the outcome is likely to be.

Colds and Flu: Variations on a Theme

    You wake up one morning with a scratchy tickle at the back of your throat. It’s nothing, you think, but by the evening you’re worried. What are you coming down with now? In all likelihood, it’s just a cold. The sore throat will persist for a few days, along with a runny nose and stuffy head. You may develop a cough. About a week after the scratchy throat began you begin to forget about the cold and by ten days it is a memory. Your body has met a small bit of protein-coated RNA called a virus, and defeated it. 

The difference between a cold symptoms and flu symptoms

    The next month another bit of protein-coated RNA called an orthomyxovirus finds its way into your nose. This time the story is very different. At noon, you are feeling well. By 4PM you have been felled. Getting up from your desk feels like climbing Mount Everest. You cannot get warm – even under a pile of blankets. Then come the muscle aches, as if you’d run a marathon. This time there is no hope of sticking to a routine – you have the flu. The worst of the symptoms fade after a week, but fatigue and lack of energy may persist for several more. Rest, time and patience eventually lead you back to health. Next year, you think, you will get that flu shot. 

The viruses that cause the problems

    The viruses that caused these two illnesses are superficially similar. They are little protein bags full of bits of RNA– technically not living things, but able to commandeer the machinery of living cells to reproduce themselves. Carried in droplets spewed into the air by coughs and sneezes of infected people, they are directly inhaled or carried into the nose and mouth on fingers from surfaces where those droplets landed. Specialized proteins on viral surfaces attach them to the cells in the upper airways. These proteins (H, or hemagglutinin and N, or neuraminidase) and their numbered subtypes (1, 2, or3) give flu viruses their unimaginative names. Swine flu virus becomes H1N1.   

    For reasons not yet understood, the body’s response to the attack of cold viruses is not as severe as it is to flu viruses. Once inside cells, flu viruses elicit a flood of proteins called interferons, which are the source of fever, muscle aches and profound fatigue. The viruses rapidly go about the business of making more of themselves, sending them out to infect more cells and generating a new wave of symptoms. In the meantime, white blood cells begin to produce antibodies that target viral surface proteins and prevent them from locking onto more cells. Eventually the tide of the battle turns and no more cells are infected. The rest of the illness -the recovery phase – involves cleanup of the remnants of the fight. 

Why flu shots don’t always work
    Flu shots use mixes of several different flu virus types to stimulate the body to make antibodies to those viral surface proteins in advance of “catching” the flu. If and when the virus invades, the antibodies are in place, ready to block the initial attachment to cells in the upper airways. Because the flu viruses that travel the world vary over time, each year’s flu vaccine is a composite of some of the currently circulating strains and may or may not be a good match to the virus that ultimately shows up.  

    Immunization is recommended for children (older than 6 months), the elderly, people in the health and teaching professions, those living in nursing homes and dormitories, and for all age groups who are at risk for flu complications, namely those with other respiratory problems, cardiac disease, diabetes and immune system impairments (including those induced by treatment of other diseases like cancer). Most adults in good health have the immune wherewithal to recover from flu and colds without complications or medical intervention. 

Complications of the flu

    The complications of the flu and of colds are similar. Both infections affect the upper airways, causing swelling and inflammation of the linings of the nose, throat and sinuses and blocking narrow passageways within. Earaches and pain in the forehead or the face develop but often resolve with simple measures like propping head up while sleeping, and taking an anti-inflammatory medication like aspirin or Advil. Unremitting pain, with or without fever, may indicate secondary bacterial infection of the ears or sinuses – the only reason for the prescription of an antibiotic during a cold. 

    Pneumonia is the most serious flu complication. Pneumonia means that the lungs’ spongy structures where carbon dioxide is exchanged for oxygen are swollen and filled with inflammatory debris. Reappearance of fever and fatigue after the flu has begun to improve may be the first sign of pneumonia. Other symptoms are chills, chest pain, shortness of breath, and dry or productive cough. Sometimes the pneumonia is caused by bacteria, but more often by the original virus or another. Pneumonia caused by bacteria, at least outside hospitals, is much less common. Prompt medical attention is in order because oxygen levels may be low. Medical attention should also be sought for other delayed symptoms like change in mental status, particularly in babies and the elderly. Occasionally diarrhea and vomiting are part of the flu and may produce dehydration.       

Why hydration is important

     Dehydration is also a result of fever, the metabolic equivalent of exercising in a warm environment. Dehydration stresses already inflamed airways. The easiest way to keep track of hydration status is to look at your urine – the darker the color, the drier you are. Aim for almost clear urine by drinking plenty of water.  

Managing fever

    Fever, while distressing, is part of the body’s defense against cold and flu viruses, which thrive in the relatively cooler temperatures of the upper airways. Some of the fever related discomfort can be relieved with a bath. Aspirin is not to be used in children with the flu because of a rare complication called Reyes syndrome, a liver failure. Tylenol is safe for them.

  What about anti-viral drugs for the flu

     Antiviral drugs (Tamiflu, Relenza. Symmetrel, and Flumadine) drugs are only effective if begun in the first 24-36 hours after symptoms begin. They lessen the duration of symptoms by about a day. Widespread use will produce increasing numbers of drug resistant strains of viruses.  

    New flu viruses appear regularly and prompt anxious comparisons to devastating epidemics of the past. Worrying about them doesn’t help. Taking care of what you can do for yourself and your contacts (see below) is your best option. 
                                                                      Useful actions to prevent colds and flu

  • Maintain good health habits throughout the year: adequate sleep and exercise, nutritious diet, no smoking, modest alcohol use.
  • Cover your nose and mouth with a disposable tissue when you cough or sneeze, with the crook of your elbow in the absence of a tissue.
  • Wash your hands with soap and water or an alcohol based cleanser after coughing or sneezing, before eating, and after being out in public.
  • Keep your hands away from your eyes, nose and mouth.
  • During flu outbreaks avoid crowded, closed environments when possible and wash hands when you come home.
  • Remember that your flu is infectious for up to 7 days and try to avoid infecting others.
  • Get a flu shot if you are in a high risk group.

Fatigue: Gentle Messenger…and Tyrant

As Supreme Court Justice Potter Stewart famously said, when confronted with a decision about what constituted pornography, the definition is hard, but “I know what it is when I see it.” An all-encompassing definition of fatigue is similarly difficult, but everyone knows what fatigue feels like. The profound lassitude that signals an oncoming flu is a gluey, mesmerizing state of mind and body that renders one incapable of remembering ever feeling good, of imagining ever feeling energetic again, or of conceiving of a desire to participate in any physical, social or mental activity beyond crawling beneath the bedcovers.  

The perception of energy failure

 Where there is life, there is fatigue. All plants and animals run on energy produced in little chemical factories (mitochondria) in every cell. The ultimate source of biologic energy is the sun’s nuclear energy, converted to usable form by plants and transferred to animals as food. The more complex the living thing, the more obvious the need for periods of rest and recovery to replenish energy. When the demand energy use outpaces the time needed for recovery, or when normal function is derailed by illness, drugs or toxins, fatigue is the name we give to what we feel, mentally and physically. To the research scientist, fatigue is a by-product of numerous little proteins (cytokines) produced by the immune system to protect us from outside invaders and internal disorders like cancer. How these proteins create the feeling of fatigue is a mystery, but there is admirable logic in a system that commandeers a patient’s energy, drive and ambition and sends him packing off to bed while an internal battle rages.  

Voluntary fatigue

Less admirable is our ability to override the biology that produces tiredness, and to become passive, cranky and sleep-deprived. In fact, most complaints of fatigue reflect the deliberate choice to ignore the symptom and would and yield to simple lifestyle changes – if one were willing and able to sleep more, lose weight, eat regular, well-balanced meals, exercise enough, manage time wisely, avoid smoking, excess alcohol, and junk food, and engage in satisfying work. In our culture these are tall orders, and a background level of fatigue is often accepted as normal. 

Evaluation of fatigue 

New, unexpected and persistent tiredness, however, may signal underlying illness or environmental stress and warrants a serious evaluation, with clear communication about exactly what fatigue means to the patient. First, a description of the patient’s normal “background energy” is important. Some people are full of energy from the day they are born. Others are inveterate couch potatoes, happy to sit and watch life go by. The feeling of fatigue that prompts one to see a doctor is, by definition, different from the patient’s normal state, but the doctor sees only a snapshot in time. Patients and families should never be shy about volunteering information about what life used to be like. 

Defining the symptom

Next, the language used by patients to describe fatigue needs to be clear. “I’m tired” sometimes means “I’m weak,” and “I’m weak” sometimes means “I’m tired,” but in the jargon of medicine, weakness means loss of muscle strength. Provided that they exert full effort, tired people can generate normal muscle power upon request, but people with strokes or nerve and muscle diseases cannot. Separating weakness from fatigue is the doctor’s first job – otherwise he may head off on the wrong diagnostic road. Description of the activities affected by tiredness and/or weakness, and characterization of changes fatigue brings to daily life are crucial to the process of diagnosis.   

Finding the source

Once a doctor understands the way fatigue affects life for a patient, he moves on to a “review of systems” – a top to bottom list of questions ranging over all the body’s organs, looking for clues to the presence of heart, kidney or liver disease, diabetes, cancer, sleep apnea, restless leg syndrome, insomnia, degenerative neurologic diseases like Parkinson’s, autoimmune illnesses like lupus or MS, chronic infections, eating disorders and problems of the thyroid, adrenal and pituitary glands. A good doctor will then delve into the lifestyle and life events surrounding the appearance of fatigue. Tiredness is a complex, high level symptom that may also originate in the mind – it is one of the cardinal symptoms of depression. 

Is it the drugs

Next comes a careful inventory of all medicines in use, prescription and non-prescription. New fatigue symptoms may parallel the addition of new drugs (even antibiotics can cause fatigue). An inventory of potential toxins and hazards in the environment may turn up a faulty furnace producing carbon monoxide or exposure to toxins such as volatile hydrocarbons that can damage the part of the brain called the cerebellum – a major player in energy balance. 

Following the clues

 Following a good, inquisitive medical history, a complete physical exam (the kind that requires undressing) may turn up other clues that suggest the need for more than “routine” tests. Fatigue is messenger bringing information about conditions ranging from minor to mortal. When not readily explained, fatigue warrants the best of our medical tools to ferret out the source of trouble. The first step though, is still a careful history and physical examination. Without these, advanced medical technological evaluation of fatigue is little better than a fishing expedition sent to sea with no information about where the fish hang out. 

                                                    The Chronic Fatigue Syndrome

Definition:

Profound, life-altering fatigue lasting more than 6 months.

May follow a viral infection, but no test abnormalities persist along with the fatigue.

Physical and mental activities both worsen symptoms.

Variety of accompanying symptoms: weakness, muscle and skeletal aches and pains, impaired memory, lack of drive, poor sleep.

Diagnosis:

No specific tests, other than exclusion of other illnesses that produce these symptoms, among others. CFS is a “diagnosis of exclusion.”

Conditions to be excluded:

Chronic infections, mononucleosis, autoimmune disorders (lupus, M.S.), hypothyroidism, low adrenal function, sleep apnea, cancer (particularly pancreatic), obesity, eating disorders, drug and alcohol abuse, major psychiatric disturbances: schizophrenia, depression. 

Heart Failure: The Price of Success

In 1953, surgeon John Gibbon undertook the first successful open heart surgery using a heart-lung machine, a pump that performs both heart and lung functions while the heart is stopped for repairs.  The pump ushered in a new era of cardiac surgery and made it possible to correct heart problems that had up until then caused premature disability and death.

In the years that followed Dr. Gibbon’s groundbreaking surgery, materials science, technology and pharmacology advanced rapidly, allowing surgery and medication to be used to treat a wider variety of heart problems, including heart attacks. Today we live in an age of coronary artery bypass surgery, clot-busting drugs,  and stents that prop open diseased coronary arteries. Advancements such as these have reduced death rates from heart attacks substantially; nonetheless, heart disease remains the number one killer of men and women in the United States, and heart failurethe constellation of symptoms that come from poorly contracting heart muscle –  is now the leading cause of hospitalization for patients over the age of sixty-five. With all of the progress that has been made in cardiovascular care, how can this be?

Why is there more heart failure now than in the past?

The answer is simple. Mortality rates are lower in the immediate aftermath of heart attacks because of the ability to dissolve clots and prop arteries open. Drugs and lifestyle management may be slowing the progression of the coronary artery disease that causes heart attacks. As a result of these advances, people no longer die as often in the earlier phases of a very long disease process which often ends in failure of the heart muscle to contract as strongly as it needs to.

If you liken cardiovascular care to home repairs, then the major advances in care ­­­have taken place in areas roughly equivalent to plumbing and electrical maintenance. Angioplasties, coronary artery bypasses, and stents are used to keep the pipes open; electronic pacemakers provide power, triggering muscle contractions in an organized fashion, while defibrillators restart the power when there are outages. A house with functional plumbing and electrical systems remains habitable remains habitable long enough for the underlying structural elements of the building, like the roof, ceilings, walls, and floors, to begin to fail. In the heart, the underlying structural element is muscle. When the muscular structure of the heart begins to fail, the signs and symptoms of heart failure appear.

Signs and symptoms

Heart muscle fibers that begin to contract less efficiently reduce the heart’s pumping capacity, preventing adequate blood flow to the major organs. The body reacts to this deficient blood flow by increasing the volume of blood in the body. It accomplishes this by retaining more salt and water, but when this happens, the blood’s increased volume stretches the failing heart muscle and damages it even further. The more the heart stretches, the less efficiently it pumps; the less efficiently it pumps, the more the body tries to boost blood flow by retaining fluids.

This vicious cycle results in what is known as congestion. Congestion occurs when the tissues, including the lungs, becoming filled with excess fluid. This fluid buildup causes swelling in the legs and abdomen and a shortness of breath. Fatigue and an inability to tolerate exercise are the heart failure patient’s constant companions. Gravity causes fluid to collect in the lower half of the body while the patient is standing or sitting, and when he lies down, it becomes redistributed, accumulating in the lungs where it can cause a telltale shortness of breath that is symptomatic of a deteriorating heart.

Causes

Age is an important contributing factor in the development of heart failure because the longer people live, the more time there is for coronary artery disease and the problems that contribute to it to take their toll on the heart muscle. Coronary artery disease deprives areas of the heart of blood and oxygen, leaving behind damaged muscle that contracts poorly and moves blood inefficiently. Smoking, excessive alcohol use, diabetes, hypertension, obesity, and lack of exercise contribute not only to coronary artery disease, but also to weakening the heart muscle directly. Less common factors involved in heart failure include viral infections that affect the heart and a variety of rare metabolic conditions that disrupt heart muscle fibers. Heart valve disease, when left untreated, can ultimately damage the heart by dilating it or causing it to thicken. However, valve disease is much less prevalent since the development of successful antibiotic treatments for childhood streptococcus infections.

Treatment

The quality and length of life heart failure patients can expect depends on how closely they adhere to the treatment plans provided by their doctors. Salt-restricted diets are a very important part of a heart failure treatment plan, and the mainstays of drug treatment plans are medications that prevent salt retention, get rid of excess water, improve the ability of the heart muscle to contract, and decrease blood pressure. Heart failure treatment treads a fine line between causing the patient’s body to retain too much and too little fluid. Drying a heart failure patient out too much can push the kidneys into failure. Too little and the lungs are liked soaked sponges, unable to exchange carbon dioxide for oxygen efficiently.  The margin of error in fluid balance gets smaller and smaller as the disease progresses and this tightening window contributes to high hospital readmission rates for congestive heart failure patients.  Physicians must monitor their patients’ weight, symptoms, electrolytes, and kidney functions more and more closely and start adding tests like chest X-rays and echocardiograms.

A variety of innovative devices and surgical procedures have been designed to cinch up dilated, failing hearts but have not succeeded in producing adequate results. Some success is being reported from the use of multiple pacemakers, which allow different segments of the heart to be stimulated in a defined order that improves the sequence of muscular contraction enough to generate greater cardiac output. Currently, bi-ventricular pacing—the separate pacing of both sides of the heart–is the most promising addition to the heart failure treatment arsenal. Cardiac transplantation remains the most difficult, expensive, and uncommon solution for a heart that has reached the end of its functional life.

Heart failure may eventually be overcome by artificial pumping devices or methods of stimulating the production of new cardiac muscle, but in the meantime, prevention is still the most desirable treatment option. Not smoking, maintaining a healthy weight and good exercise habits, sticking to a balanced diet of fresh foods, getting adequate sleep, and managing stress well are all cheap and valuable ways to invest in your heart’s health.

 

Body Talk

       When I lived in Minneapolis, I loved Auto Talk, a call-in radio show from St. Paul, MN. The hook that caught me the first time I heard the host Paul Brand and his listeners was the show’s similarity to the doctor’s office. 

        Except for the subject, the conversation could have been between doctor and patient. Each caller described his car’s symptom. Mr. Brand listened carefully, but sometimes broke in to ask a few questions, just like a doctor taking a patient’s history. Then he described a variety of possibilities that might account for the car’s symptoms – a differential diagnosis. Mr. Brand clearly had the advantage of expertise, but his callers were knowledgeable participants, already the “wiser customers” he hoped to make them by “helping them understand more about their automobiles.” Substitute bodies for automobiles and you’ve got part of a mission statement for the doctor’s office. 

        In our new medical world, patients are urged to be active participants in their own care. The paternalistic doctor is out of fashion and the patient is an informed “consumer.” Like the callers to Auto Talk, who have a good working knowledge of automobiles, you are now supposed to understand your body and have opinions about what to do with your problems. But it’s hard to pretend you’re just seeking ordinary repair service from the doctor, so the consumer analogy breaks down and communication suffers.  

       When you go to a doctor you are a captive audience, not a car owner. You are there because you fear something is wrong with you. And unlike the car owner, you can’t get an engine overhaul or a new vehicle. The stakes are higher for a patient than a consumer, and the unknown is scarier. 

       Unlike Mr. Brand, who could close down his microphone at the end of the hour, the doctor has ongoing worries. He is responsible for the patient, he annoys the insurance companies who pay him, and he risks lawsuits every day. Right from the beginning, an adversarial tinge colors the relationship between doctor and patient. The conversation is more guarded and less collegial than it is on Auto Talk. 

       The callers to Auto Talk were a self-selected group who were interested in the language and mechanics of automobiles. Patients often escape any interest in their bodies until something goes wrong. And when they are sick, they are not likely to embark upon a home study course in anatomy and physiology. The easy flow of conversation that happened on Auto Talk runs an obstacle course of fear and language obstructions in the doctor’s office.  

        Mr. Brand’s audience was schooled, at least partially, in car language, but in the medical setting, the doctor has to be a translator who is sensitive enough to recognize when he’s gone off and left his patients behind. Medical language sounds complicated, but is just shorthand – a few words in medicalese convey paragraphs of information to anyone else involved in the patient’s care. 

     Practical knowledge about their own cars also helped Auto Talk callers understand where Mr. Brand’s questions were headed. Sometimes patients think doctors are rude when they interrupt and shift directions, but studies have shown that within thirty seconds of the start of conversation between doctor and patient, the doctor is already sifting the information he is hearing and seeing, and beginning his differential diagnosis. Be patient with him. He is just leaping to the next logical symptom. 

       Being an active participant in your medical care doesn’t mean you have to learn medical language or understand the relationship of seemingly unrelated symptoms. But you can be like an Auto Talk caller and know how to describe your symptoms. This requires no special language – just observation. Let’s say you have a pain in the abdomen. Can you tell where it is? What does it feel like? Can you compare it to another type of pain? How often does it happen? How long does it last? Is there anything that you can do to change it (like turning over, or burping)? What makes it worse? What makes it better? When did you first notice it, and what were you doing at the time?   

      AutoTalk callers knew a lot about their cars’ histories. You can be prepared to give your history without much trouble if you keep a written list of the medical problems and treatments you’ve had, and of all the medicines that you take (including over the counter pills). Nothing gets overlooked, and sometimes the answers lie in these details. 

      Because illness is distressing, concentration on a discussion is difficult. Slow down, take deep breath, and listen as carefully as you can. Above all, ask questions. Ask away until you have a clear idea what the doctor thinks your problem is and what the plan of action is. Most offices provide you with educational material and written instructions, but it is OK to take your own notes, and to bring someone trusted with you to help. 

      Mr. Brand’s goal was to expand knowledge so people get “longer service life” out of their automobiles. The word doctor means teacher, and the goal of medical care is longer service life of the body. Who better to guide patients to good quality information, rather than information designed to sell a drug or a product? What better way to facilitate communication than both parties attempting to build knowledge? Call it Body Talk. 

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