The Headaches that Predict Catastrophe

One of the most treacherous problems a busy emergency room physician faces is headache. “Headache” is a very common symptom, different from focal head pains attributable to sinus, eye or ear problems. While very painful and sometimes associated with nausea and vomiting, the vast majority of headaches, even if frequent and debilitating, are benign. They do not signify underlying illnesses or impending danger. But the emergency physician cannot afford to be wrong about the rare headache that predicts oncoming catastrophe and provides a chance to intervene.

Two broad categories

Catastrophic headaches fall into two broad categories. The first category includes “space-occupying lesions” such as tumors, hemorrhages, abscesses, and hydrocephalus (known commonly as “water on the brain”). The second category involves infectious and autoimmune problems that produce inflammation, triggering pain receptors in the membranes surrounding the brain and its blood vessels. Catastrophes avoided by successful interventions in both categories include death, permanent brain damage and blindness.

Tumors and abscesses

The most common fear about a bad headache is that it is caused by a brain tumor, but tumors usually produce other symptoms, involving speech, thinking, coordination or vision before they produce headache. Since the brain tissue itself has no pain receptors, tumors cause headache when they distort surrounding membranes or blood vessels, which have pain receptors. Tumor-related headaches worsen with positions and activities that normally cause the pressure in the veins in the head to rise – coughing, sneezing, lying down, straining at a bowel movement or lifting something heavy. As tumor size and pressure increase, nausea and vomiting appear. Occasionally, brain abscesses – pockets of infection surrounded by capsules -may mimic tumors. They usually come from blood infections seeding bacterial or fungal organisms into the brain.

Hemorrhages in the brain

Brain hemorrhages occupy space and increase pressure in the head. Deep small blood vessels, damaged by high blood pressure or arteriosclerosis, are usually the culprits. While these intracerebral hemorrhages can cause sudden headache, stroke-like symptoms such as paralysis, confusion, trouble speaking and loss of consciousness occur first or soon after the onset of headache.

Hemorrhages outside the brain, but inside the head

Headaches are also a symptom of epidural and subdural hematomas – collections of blood that accumulate over the surface of the brain hours to weeks after some closed head injuries (meaning no skull fracture). The history of injury, even seemingly trivial injury in an elderly patient, is crucial to correct evaluation of these headaches and there may be no other accompanying neurological symptoms. A head blow in the temple, where the skull is the thinnest is a common history. Young children and older adults are more susceptible to epidural hematomas (located between the inner skull and the the dural membrane over the brain) than those in between those age groups. Both epidural and subdural (between the dural membrane and the surface of the brain) collections of blood usually require surgical removal, sometimes as an emergency if symptoms such as change in level consciousness appear. Actor Liam Neeson’s wife Natasha Richardson did not survive an epidural hematoma incurred in a skiing related fall in 2009.

The “sentinel headache” of the aneurysm

Bleeding from brain aneurysms – weak spots at branch points of arteries – can be immediately catastrophic, even causing sudden death. But a tiny, warning leak before an aneurysm actually ruptures may cause a “sentinel headache” which allows time for life-saving surgical repair to prevent the oncoming, big rupture which typically occurs sometime in the next 10 days. A sentinel headache is sudden and severe pain involving all or part of the head, It is sometimes described like a “thunderclap.” As the little warning squirt of blood dissipates in the spinal fluid around the base of the brain, the headache dulls but a peculiar, longer-lasting pain may appear in the middle of the upper back, usually worsened with movement and probably indicating irritation from blood in the spinal fluid around the spinal cord. Diagnosis involves brain imaging with dye to study the arteries, and possibly a spinal tap to make certain bleeding has occurred. Unruptured cerebral artery aneurysms are found incidentally in 2% of autopsies so the problem is not rare.

Hydrocephalus

Hydrocephalus is a rare cause of headache, but one that should never be overlooked. The rise in pressure in the head comes from spinal fluid being trapped in the ventricles, hollow structures in the center of the brain where spinal fluid is made. Normally the spinal fluid circulates out of the ventricles via a very small channel, and bathes the surface of the brain and spinal cord before being absorbed into special veins at the top of the head. If flow is blocked, the ventricles begin to enlarge putting pressure on the surrounding brain. Most times, the onset of hydrocephalus is gradual, with headache, nausea, vomiting and balance problems gradually increasing. Unrecognized and untreated, obstructed spinal fluid flow leads to lethargy, coma and death, within 24 hours if the obstruction is sudden. Causes of obstruction include congenital anatomical abnormalities, tumors blocking the ventricular outflow tracts, scarring of these passages by inflammation from past meningitis or bleeding. Hydrocephalus most often requires surgical intervention to either remove the obstruction or to place a shunt around it, allowing cerebrospinal fluid to escape from the ventricles.

Headache from infection

Headache producing infections mainly involve the meninges, the membranes covering the brain and the spinal cord and are caused by viruses, bacteria or fungi. Viral and bacterial meningitis both cause severe headache, neck pain and rigidity and photophobia – inability to tolerate bright light. Movements of head and trunk and even eye movements are painful. Someone suffering from bacterial meningitis has a high fever, looks extremely ill and deteriorates rapidly. Identification of the infection type requires spinal fluid, obtained via spinal tap – insertion of a large needle into the spinal canal in the low back. Antibiotics are lifesaving. Viral meningitis, though painful, is less dramatic, and gets better on its own. Fungal meningitis is rare and much slower and less dramatic in its presentation than bacterial meningitis. It most often occurs in people who have impaired immune systems and requires prolonged treatment with antifungal drugs.

Non-infectious inflammatory headache: temporal arteritis

Headache from a non-infectious inflammatory condition called temporal arteritis usually presents itself in the seventh or eighth decade of life as a constant, often one-sided pain. Other symptoms that provide clues to this diagnosis are pain in the jaw muscle, especially with chewing, and tenderness of the artery just under the skin of the temple – the origin of the name for auto-immune inflammation that affects the arteries that supply the skull and brain with blood and can cause blindness and strokes. Diagnosis is confirmed when a blood test called ESR (erythrocyte sedimentation rate) is elevated and a temporal artery biopsy shows characteristic inflammatory cells in the artery wall. Treatment with steroids like prednisone, undertaken soon enough, prevents blindness and takes the headache away, but must be continued for many months.

A very useful question

One of the most useful questions an emergency room physician, or any other professional evaluating a headache complaint can ask the patient is “How worried are you about this headache?” People know themselves and have an innate sense about the nature of their symptoms. They will very often know the difference between a catastrophic headache and all the others.

Posted by medical plaintalk

Physician turned medical writer.

Probiotics: Manipulating Your Internal Ecosystem

The human body is an ecosystem harboring numerous different species living in delicate balance, well-adapted to each other and to their physical environment. The creatures that thrive on our skin and in our noses, mouths, urogenital tracts and guts are microscopic organisms – mainly bacteria, fungi and bacteriophages (viruses carried by bacteria). These organisms comprise the human “microbiome” and perform valuable services for us, breaking down food, making vitamins and other chemical compounds that we absorb, teaching our immune systems how to recognize invaders, and maintaining bowel health. Their genes interact with our genes, up-regulating and down-regulating them as we change our diets.

Research relating the the invisible world of the microbiome to physical states of health and illness is still in its infancy, but has produced interesting data and useful observations about attempts to restore microbiome composition after disruption by illness and antibiotics. Outside this world of esoteric research, entrepreneurs have leapt ahead of the facts, supplying millions of people who wish to better their health with supplements called probiotics, pills containing “living microorganisms, which when administered in adequate amounts, confer health benefits on the host.”

Not a new idea

The idea of manipulating the body’s microorganisms to improve health is not new. In 1908, Nobel prize winner Elie Metchnikoff, the “Father of Immunology,” theorized that the large intestine was a cesspool where putrefaction by bacteria produced autotoxins that aged the body. While some believers advocated removing the colon or administering repeated enemas to cleanse it, Metchnikoff thought that Lactobacilli, bacteria found in the yogurt consumed by long-lived Bulgarians, could battle the putrefactive bacteria, and that consumption of the yogurt, along with other ascetic practices like avoidance of alcohol and intoxicants, would prevent dementia, illness and premature death. Like yogurt, other fermented, bacteria-laden foodstuffs such as kefir and sauerkraut have long been advocated for general good health.

Experimental evidence?

There is tantalizing experimental evidence that the interior microbial world has previously unsuspected ties to overall health. For instance, in germ-free mice, introduction of specific bacteria into the gut will alter energy usage because the bacteria digest incoming food. The mice get fatter on the same amount of food they were fed in the germ-free state because they absorb more of it. Bacteria also produce substances which act like neurotransmitters and communicate with the brain via the gut’s neural network. And they modify the action of their genes to match the types of food we eat, which in turn modifies food absorption and immune system function.

Genetic tools speed modern microbiome research

High speed DNA analysis is the modern tool which drives microbiome research. No longer do scientists struggle with culturing and identifying the multitude of bacterial types that reside in the human body. Based on microbial DNA sequencing of samples from human bodies, we know that we carry over 3.3 million bacterial genes, vastly more than our own 22,000 genes). There is far more diversity between humans in terms of the genetics of the organisms they carry than there is in their genetic profiles – and enough stability in each person’s microbiome to create unique microbial DNA profiles, which can be identified like fingerprints on surfaces people touch. There are even identifiable differences between the fingerprint profiles from an individual’s right and left hands.

Fecal transplants: the ultimate probiotics

The best scientific information about manipulation of the microbiome in the quest for better health comes from the ultimate type of probiotic – the so-called fecal transplant. Transfer of fecal material from one person’s gut to another’s was first tried in the 1950s. In this experiment, a patient suffering severe colitis was spared surgical removal of the colon when restoration of a normal mix of bacteria, as well as everything else in contained in the stool sample used for the transplant, quelled the toxic bacteria eating away his colonic lining. Since that time, fecal transplantation has been 90% successful in treating the severe and often recurrent colitis and diarrhea produced by the bacterium clostridium difficile.

The complex nature of fecal material

Fecal material contains bacteria, viruses, bacteriophages – the viruses that bacteria can transfer among themselves and to the host, other types of microorganisms, and all the chemical products of the metabolic processes of all these living creatures. Each stool donor has a unique microbial profile, as does each fecal transplant recipient. Donor stool is screened for drug resistant and abnormal bacteria, prepared as a slurry and introduced into the colon via colonoscope, or into the stomach or small intestine via a tube. Capsules that resist the acid and enzymatic environment of the upper GI tract also show some promise.

Probiotics: less complex mixtures of living organisms than fecal transplants

Like fecal transplants, probiotics aim to create a healthier balance of bacteria in the gut, but they are capsules containing a few types of freeze-dried bacteria harvested from cultures in labs. When swallowed and exposed to the warmth and moisture of the body’s interior they spring to life. Sold as supplements, probiotics are not subject to FDA quality control.

Probiotics have been studied as treatments for antibiotic-induced diarrhea, allergies, autism, metabolic syndrome, autoimmune ulcerative colitis, Crohn’s, disease, infectious colitis, constipation, traveler’s diarrhea, periodontal disease, and more. The studies are fraught with problems that make most of them inconclusive at best. But as preventives for antibiotic0induced diarrhea and clostridium difficile diarrhea, probiotics may be helpful and are generally not harmful for otherwise healthy people. Theoretically, people with depressed immune systems could contract an infection from one of the organisms included in the product. There has been at least one neonatal death attributed to a contaminated probiotic.

Do the introduced bacteria survive?

A recent, carefully designed study from Israel assessed whether or not probiotic bacteria took up residence in the colon after ingestion. In some people, called persisters, the probiotic bacteria can be found in the recipient, but in others, called resisters, none of the probiotic bacteria survive. The type of bacterial populations already living in the gut make the difference. In addition, another good study demonstrated that probiotic use actually delayed the return of normal bacteria to the colon after a course of antibiotics.

Much work remains in the investigation of the human microbiome and in attempts to improve health by manipulating it. What is clear so far is that each person’s microbiome is unique and that success in understanding and manipulating it will require individualized evaluation. Most probiotic use at this time is a one-size-fits-all approach, done for non-specific reasons. Similar to Metchnikoff’s Bulgarian yogurt.*

*modern science shows that the lactobacillus in the yogurt does not survive the trip through the gut to the colon.

Posted by medical plaintalk

Physician turned medical writer.

Tuberculosis: The Long Pandemic

In late 2012, a Nepalese man began a three month-journey, on foot, by car and boat, and in an airplane, through South Asia, Brazil and Mexico, and into Texas. He brought with him an infection called XDR-TB, short for extensively drug resistant tuberculosis, a disease still relatively rare in the US, but one that public health officials fear because it is spreading across the world. We have become complacent about TB because it has been successfully treated with antibiotics since the 1950s and because most tuberculosis cases occur in underdeveloped countries where malnourished and sick people with weakened immune systems live in crowded and unsanitary conditions. But with easy global travel and spreading antibiotic resistance, especially on the Eastern border of Europe and in Africa, China and India, more awareness of this ancient disease is needed again in areas of the world where improved living conditions have made TB uncommon and unknown.

A long history

Three-thousand-year-old writings from China and India, passages in the Old Testament, and the writings of Hippocrates all describe the affliction we call tuberculosis. The disease became a scourge as more and more people crowded into urban centers in northern climates in the middle ages. Between the 1500s and 1800s, hundreds of millions of people in Western Europe, England and the eastern US died of TB, then called consumption and attributed either to a “malignant miasma” in the air or to hereditary constitutional weakness. Squalid living conditions, poor indoor ventilation and malnutrition common during the early industrial revolution facilitated the spread of the disease, which in 1882 was finally proven to be caused by a bacterium, Mycobacterium tuberculosis. When living conditions began to improve in the early 1800s the death rate began to decline, but a cure awaited the development of antibiotics in the mid-twentieth century. The goal of eradicating TB, however, has not been achieved.

Latent vs active infections? The immune system decides.

Anyone can be infected with the TB bacteria, acquired by inhaling the respiratory droplets of someone who has an active infection in their lungs. Inhaled TB bacteria are captured by cells that scour the airways for invaders. The bacteria reproduce themselves inside those cells, eventually killing them and exciting an immune response that in 90% of people will clean up the infected area, called a “tubercle,” in a process called caseating necrosis because the dead tissue resembles crumbled cheese. The tubercles may leave small scars in the lung, visible on chest X-ray, without ever having caused any symptoms of illness. Infection in these immuno-competent people, the vast majority, is called latent TB, a condition that affects almost a third of the world’s population, including 13 million people in the US.

In 10 % of people who get infected with the TB bacteria, the immune response is insufficient. Active tuberculosis is the result. Caseating tubercles may grow to large size and collapse producing cavities in the lung. Tubercles that erupt into the airways allow surviving bacteria to spread to other people in sputum and respiratory droplets. In addition, bacteria may travel to other parts of the body via the lymphatic system, setting up infectious nodes in almost any tissue. Typical symptoms of active tuberculosis develop over weeks to months and include chronic cough, night sweats and fever, weight loss, weakness, fatigue, and skin pallor. Tubercles in various organs and lymph nodes give rise to local symptoms from swelling and inflammation.

Latent infections come alive

Latent TB can reactivate and become active TB if the carrier’s immune system weakens – a result of other disease such as HIV, drug treatment that suppresses the immune system, or just deterioration of health that accompanies drug use or poor living conditions. Ten million cases of active infection occur each worldwide year.

Before antibiotics: high altitude and collapsing lungs

In the 1840s a botany student who suffered from TB traveled to the Himalaya mountains and came home to report his cure, setting in motion the sanatorium treatment for which high altitude locations such as Davos Switzerland and Denver, Colorado became renowned. Much later, scientific work showed that the mycobacterium tuberculosis grows poorly at low oxygen pressures, a fact that may well have added to the other health and nutritional benefits of sanatorium life. Attempts to put infected parts of lungs “to rest” by collapsing them with injections of nitrogen into the chest began in the 1880s. German Author Thomas Mann memorialized this procedure, called an artificial pneumothorax, in his novel The Magic Mountain. The treatment method continued well into the 1940s, when the development of antibiotics finally offered a cure for TB.

Not the usual antibiotic treatment

Antibiotic treatment of TB is not easy. Patients must take two to four drugs on a strict schedule for 6-9 months and tolerate some unpleasant side effects like nausea. Until their sputum is free of TB bacteria – which can take several weeks – they must be strictly isolated. Caretakers benefit from proper mask wearing because the tuberculosis bacteria is larger than N95 mask pores. Because drug resistance has been a result of poor compliance with the drug regimens, strict monitoring and observation of patients is necessary. Often drugs must be taken under direct observation. Once drug resistant disease occurs, treatment becomes more complicated and prolonged, requiring trials of different antibiotics, with even more need for isolation of infectious patients and close supervision throughout the entire course of treatment.

Testing and vaccines

A tuberculin skin test, when positive, indicates prior infection with tuberculosis bacteria, and therefore latent disease in someone who has no symptoms. Chest X-ray and chest CT, as well as collection of sputum for microscopic analysis and culture are the mainstays of diagnosis in active disease or if someone with a positive skin test has any suspicious symptoms.

The only vaccine for TB, used since 1921, is made from a weakened bacterium similar to the TB bacterium. Its acronym BCG is short for the virus name (Bacille Calmette Guerin). BCG reliably prevents neonatal disseminated forms of TB such as meningitis, but is much less effective in preventing the adult respiratory form of TB, which is the usual version beyond childhood. It has not been regularly administered in the US because most people handle primary infections easily. However the spread of drug resistant forms of TB may change that recommendation, especially for people regularly exposed to patients. In the meantime, work on new vaccines employing new technologies continues.

Drug resistance is spreading

TB was on the decline in the US until the 1980s, when HIV disease appeared, devastating the immune systems of its sufferers and making them susceptible to active TB. With better treatment of HIV, TB is on the decline again, but popping up increasingly in the homeless population, particularly where they congregate indoors in crowded shelters. Recently, cases of drug resistant TB have occurred in people who had never been treated, meaning that the drug resistant bacteria are spreading, not just evolving in treated patients. In eastern Europe 30% of new TB cases are now resistant to many of the TB drugs. The traveler who appeared in Texas with XDR-TB was a warning. We need robust public health measures to monitor infectious diseases, improve sanitation and living conditions as much as we need development of new antibiotics.

Posted by medical plaintalk

Physician turned medical writer.

Dyspnea (trouble breathing): A symptom with many causes

A baby enters to the world with collapsed, fluid filled lungs. Within 10 seconds, he gasps, takes a noisy breath and completes his transition to the outer world. From that point, he will inhale and exhale air over 8 million times a year until he takes his last breath at death. Breathing is his link to life, much as his umbilical cord was the link when he was in the womb. As long as his heart and lungs remain healthy and the muscles and bones his chest can move normally, he will maintain a comfortable, laissez-faire relationship with his breathing, seldom paying much attention to the never-ending process of taking in oxygen and getting rid of carbon dioxide. Strenuous physical activity will make him notice his breathing and he will learn the physical limits beyond which breathing harder and faster is ineffective. While he will experience discomfort with breathing at those limits, he will not feel fear or distress because he understands that his gasping for air is a normal response and that he will recover promptly when he rests.

Words used to describe trouble breathing

But when there is trouble somewhere in the respiratory system, the act of breathing becomes distressing in ways that and prompt a variety of different descriptions: “I feel short of breath.” “I can’t catch my breath.” “My chest is tight.” “I’m smothering.” “I’m suffocating.” “I can’t take a deep breath.” “I can’t breathe out all the way.” “Breathing is hard work.” “I need to more air.” Doctors use one word to encompass all of these descriptions – dyspnea, defined as abnormally uncomfortable awareness of breathing. Dyspnea is not a diagnosis but a symptom of many different types of respiratory problems. Diagnosis requires discovering where the trouble is in the normal chain of events that make up one breath.

The drive to breathe

The first part of a normal breath is the drive to breathe – a message from the brain to the muscles that increase the volume of the chest. The ribs move outward and the diaphragm between the chest and the abdomen moves down. The chest cavity expands, much like a fireplace bellows, sucking air down the trachea and the bronchial tubes into the lungs. In the next step, oxygen is absorbed into the blood and carbon dioxide is expelled from it. This gas exchange takes place in the spongy tissue of the lungs, in tiny air sacs called alveoli where red blood cells flow in single file though tiny capillaries. After 3-4 seconds, the muscles relax, the chest cavity diminishes in size and air rushes back out. Normal breathing goes on automatically, beneath conscious awareness unless the body demands more gas exchange because of increased exertion.

The drive to breathe increases when the body’s demand for oxygen goes up. “Hard breathing” from exertion is not distressing or indicative of illness unless it occurs in someone who has been very fit and previously more capable. Low oxygen pressure at high altitude also stimulates the breathing drive, but true dyspnea is a sign of altitude sickness and need for immediate treatment and evacuation to lower altitude because of fluid in the lungs. Anxiety and fever increase respiratory drive, as does hyperthyroidism, producing variable awareness of rapid breathing, but little discomfort.

The highway air movement follows

Moving air in and out of the lungs is the next part of normal breathing and a common source of true dyspnea. Infections, chronic inflammation from allergies, cigarette smoke or other environmental toxins can narrow and partially obstruct the trachea and the bronchi. Symptoms include coughing, wheezing and faster breathing to compensate for less air moved with each breath. Breathing “seems like hard work.” Sometimes bronchial spasm from inflammation makes it difficult for people to exhale fully. They have a sense of not being able to empty the air from their lungs and as a result get the feeling that they cannot inhale enough on their next breath. Asthma is the typical illness which causes this type of dyspnea.

Muscle disorders like Lou Gehrig’s disease, overall weakness from chronic illness, or paralysis from spinal cord problems can limit air transport by limiting chest wall movement. Obesity causes breathing problems because even normal muscle may not be strong enough to move the chest wall buried under heavy weight.

The deep reaches of the lungs where the work is done

Farther down into the lungs, dyspnea comes from impaired gas exchange and feels like air hunger – no matter how fast the breathing rate is, there still seems to be insufficient air. Lung infections like viral and bacterial pneumonia, and chronic inflammatory disorders that produce lung scarring are the typical culprits. Cough, fever and rapid onset of dyspnea are clues to pneumonia. Gradual onset of dyspnea is more common in the inflammatory scarring and in smoking related lung disease, which causes both obstruction to air flow and loss of the alveoli where gas exchange occurs.

Poor blood flow through the lungs can be the culprit

Normal breathing also depends on the heart, which is the pump that pushes blood through the lungs for gas exchange. A failing heart makes blood flow too sluggish for adequate gas exchange during each breath, causing a sense that air flow is inadequate and making breathing rate go up. People who have cardiac dyspnea also describe feeling suffocated or smothered, especially if fluid begins to leak from the blood into the lung tissue. Gravity influences the symptoms which worsen with lying down and improve with sitting up.

Pulmonary emboli, clots that form in the legs or pelvis and break off and travel upstream, can cause severe and sudden dyspnea by lodging in and blocking major blood vessels in the lungs. Air reaches the lung segment where the clot is lodged, but gas exchange doesn’t occur because no blood is getting through. Large clots can be fatal immediately.

Should you develop dyspnea, seek help and try to provide a good history of your symptoms. Symptom history is very important in diagnosis and accurate diagnosis is crucial to proper treatment. The goal of treatment, of course, is a return to the comfortable lack of awareness of breathing that should accompany you from cradle to grave.

Posted by medical plaintalk

Physician turned medical writer.

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.

Morning Foot Pain: Plantar Fasciitis

“.as we know, there are known knowns; there are things we know we know. We also know there are known unknowns; that is to say we know there are some things we do not know. But there are also unknown unknowns—the ones we don’t know we don’t know.” Donald Rumsfeld former US Secretary of Defense

In medicine, what we “know” changes regularly as long as curiosity keeps opening doors. For many decades, the complaint of pain in the bottom of the foot, just in front of the heel bone and always worse with the first few steps of the morning or after prolonged periods of inactivity, fell into the “known known” category. Doctors and physical therapists confidently made diagnoses of plantar fasciitis, certain there was inflammation in the plantar fascia, the band of tough fibrous tissue that spans the bottom of the foot. The condition was common, especially in runners, in people who spend a lot of time standing on hard surfaces and in post-menopausal women. Most of the time it resolved but there were enough prolonged and vexing cases that did not get better with anti-inflammatory medications and rest that some practitioners began to suspect that plantar fasciitis was a “known unknown” – maybe the cause was not so simple as the inflammation that they postulated. After all, no one had actually looked at the troublesome tissue under a microscope before.

Plantar fascia gets an inspection

In 2003, a Philadelphia podiatrist and pathologist, Harvey Lemont, took microscopic samples of the plantar fascia from patients undergoing surgical release of their presumably inflamed connective tissue. In all 50 samples he found no evidence of inflammation. But the tissue was not normal. The collagen structure was disorganized and degenerated, as if it had been deprived of sufficient blood flow. Some samples contained crystals from prior cortisone injections, common treatment for plantar fasciitis, but by 2000 known to carry significant risk of causing the plantar fascia to separate from the heel bone. Degeneration of plantar fascial structure, a previously unknown unknown, was discovered, and that prompted a change in the name plantar fasciitis to plantar fasciosis, a term which indicates chronic structural disruption but not inflammation.

Lack of inflammation prompts new thinking

Lack of inflammation in Dr. Lemont’s pathologic examinations explained the failure of conventional treatment many cases of plantar fasciitis. And his work raised significant questions about the cause of the problem. Why does the plantar fascia begin to degenerate? What exactly hurts? Is it the bone where the connective tissue attaches? Is it the connective tissue itself? Study of the feet of non-shoe wearing cultures in which our most common foot problems are practically non-existent, and more attention to foot, leg and gait biomechanics began to yield some different ideas, not only about the heel pain syndrome, but about bunions and hammertoes.

Are shoes the problem?

When we are babies and young children, our feet are widest at the tips of the toes. By the time we wear conventional shoes for decades, with shallow, narrow and tapered toe boxes and elevated heels (even running shoes have a 1-1.5” heel elevation), the big toe begins to curve toward its mates, which begin to curl under. The muscle that normally pulls the big toe away from the other toes is pulled inward and weakens because of inactivity. What does this have to do with the plantar fascia? The big toe muscle runs from heel to toe on the foot’s inside edge, right over the artery near the heel that supplies blood to the plantar fascia. Pulling it inward narrows the artery and decreases blood flow to the plantar fascia. It is possible that morning heel pain is ischemic pain, from lack of sufficient blood flow while the foot is dropped down during sleep. Gradual Improvement in the pain with walking may reflect better blood flow with activity, but over time insufficient blood flow takes a toll on the integrity of the tissue in the plantar fascia, adding pain from stressed attachment to the heel bone.

Wimpy foot muscles

For many years people with plantar fasciitis were told they had collapsed arches and flat feet. Or high arches and no flexibility. Or that they pronated – walking on the inside of their feet. Or supinated, walking on the outside of their feet. The treatment was external support with rigid orthotics. But feet are very individual in their structure, and there is little solid evidence that arch height causes problems. Much more evidence implicates weakness at the ends of the arch – the toes and the heels, which bear the weight of the body and are supported by muscles in the feet and in the lower legs.

A shift in treatment plans

Treatment of the heel pain syndrome is shifting to restoration of strength and flexibility in the foot. The plantar fascia functions as a windlass, a pulley that adds to the arch strength when the foot lifts at the heel and bends at the big toe joint to propel the body forward. The goal of therapy is not to stretch that windlass, but to realign the big toe and strengthen the not only the foot muscles that flex the toes and the sole, but also the muscles of the lower leg, the knee and the hip. The toes are coaxed to flatten out and spread by stretching the top of the foot and the front of the ankle and wearing toe spacers. (Useful resource below.)

In the acute phase of plantar heel pain, some external support of the foot under the arch often helps, as does a boot that keeps the foot from dropping down in bed at night. But these aids are temporary while the work of regaining foot strength and flexibility gets under way. It can be difficult to transition from elevated heels to flat shoes, and that process is almost like training for a new physical activity – short bouts at first, gradually increasing over time.

Improvement takes patience, persistence and consistency. All footwear needs to change to shoes with wide, deep toes boxes, flexible soles at the forefoot, and no elevation between heel and toe. Perhaps we will find more unknown unknowns and a way to combine healthy feet with fashionable shoes, but at the moment, the known knowns suggest that changing fashion norms to align them with natural foot function is more likely to be successful.

Resources:

https://naturalfootgear.com

Foot Conditions

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.

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