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bonnieh

sodium deficiencies

Posted by @bonnieh in Just Want to Talk, Dec 9, 2011

there is only 10% of the worlds population that has this rare disorder. i am starting discussion because i am one of those people. if anyone has any tips or concerns on this disorder maybe we may be able to find some solutions to help this disorder to improve. come chat with me i would like to hear all comments and ideas.

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bonnieh

Posted by @bonnieh, Dec 9, 2011

how do you treat your sodium deficiency?

bonnieh

Posted by @bonnieh, Dec 10, 2011


Could alcohol abuse cause hyponatremia?Improve
In: Alcoholism, Addictions [Edit categories]
Answers.com > Wiki Answers > Categories > Health > Addictions > Alcoholism > Could alcohol abuse cause hyponatremia? Answer: Improve



Alcohol consumption inhibits the release of a hormone (ADH) that normally causes your body to hang on to the water it needs. Since the hormone is inhibited, your body dumps water (urine). In the body, water and sodium travel together, so with the water, the person is dumping sodium. Additionally, typically alcoholics don't have the best nutrition so they are not getting the sodium they need in their diet, so that may add fuel to the hyponatremia fire. Hope this helps.



Read more: http://wiki.answers.com/Q/Could_alcohol_abuse_cause_hyponatremia#ixzz1g9Y2Vjkr

bonnieh

Posted by @bonnieh, Dec 13, 2011

i still yet need to go to a specialist to fnd out what ty ypnatremia i have. i do knowthat minewas cased by a medicinal couteraction in my system from a psychiatric drug and also possibly toomuch fliud intake. i used to drink alcohl ut have been sober for over 1 year n and i found out i had hypontreia back in february of 2001. i have been strugglingt find ways to boost up my sodium since then. i was in critical shape when i found out i had hyponatremia. my sodium level was down to 124. i lost functions in my fingers and my face was as white as a sheet. my speech was even slurred. my eyes looked distant and also started to roam almost what seemed into different dirrections. my eyes are better now, my speech is still somewhat slurred due to the medication i am on now which is improving daily.my sodium is now up to 132 and slowly climbing. i went to a doctor and we searched out online what type of ways i could boost up my sodium, we searched online for many different sites for low sodium and kept on finding ways to only lower it we found one site that had a list of foods that are high in sodium and i just keep trying to improve my sodium as the days go by. i was quite surprised when i found out i would be able to eat what would kill most people with high blood pressure. the only thing i have to becareful about is to not pack on the pounds as i try to get my sodium back up to the ranges its supposed be which is at 135-146. that is the average normal range as far as i know. do you have any further suggestions on how to highten my sodium? if so would you please share on how you do it so that way we can possibly go on this journey together into good health?

bonnieh

Posted by @bonnieh, Dec 13, 2011

if you would like to share your experience at any tme please do so. im always interested in hearing and sharing experience strength and hope.

bonnieh

Posted by @bonnieh, Dec 26, 2011

Trileptal may lower serum sodium levels (hyponatremia), and symptoms of hyponatremia may develop if
the sodium level is not normalized. The body’s sodium concentration is regulated by the mechanisms of thirst,
hormones (e.g., antidiuretic hormone), and the kidneys. Disturbance of sodium balance can disrupt many of
the body’s physiological functions, with serious clinical consequences. Usually, Trileptal-induced hyponatremia
is mild and produces no symptoms (asymptomatic), but in clinically significant hyponatremia, symptoms
may include loss of appetite, nausea and vomiting, confusion, lethargy, headache, and agitation. Individuals
who are also receiving medications known to decrease serum sodium levels (e.g., thiazide diuretics) or those
with a medical condition that disrupts sodium balance may be particularly susceptible to hyponatremia during
treatment with Trileptal. The serum sodium levels of patients who are taking Trileptal should be monitored
routinely, especially during the first 3 months of treatment, when hyponatremia generally occurs.

bonnieh

Posted by @bonnieh, Dec 26, 2011

The sympto ms of hyponatremia or wat er intoxicat ion when plasma sodium fall s
below 120 millieq uivalent per lit er (meq/ I) inclu de: dizziness, headach e, lethargy,
mental confus ion, mental slowing, weak ness, loss of apatit e, and hosti lit y. Neu rologica
l ab normalit ies, stupor, convulsions, a nd coma, domina te as th e sodium level fall s
below 110 meq /I

bonnieh

Posted by @bonnieh, Jan 12, 2012

The body obtains sodium through food and drink and loses it primarily in sweat and urine.

bonnieh

Posted by @bonnieh, Jan 12, 2012

Syndrome of Inappropriate Secretion of Antidiuretic Hormone

Syndrome of inappropriate secretion of antidiuretic hormone (SIADH) develops when too much antidiuretic hormone is released by the pituitary gland, causing the body to retain fluid and lower the sodium level by dilution
Pain, stress, exercise, a low blood sugar level, and certain disorders of the heart, thyroid gland, kidneys, or adrenal glands can stimulate the release of antidiuretic hormone from the pituitary gland, as can the following drugs:

ChlorpropamideSome Trade Names
DIABINESE
(which lowers the blood sugar level)
CarbamazepineSome Trade Names
TEGRETOL
(an anticonvulsant)
Vincristine (a chemotherapy drug)
Clofibrate (which lowers cholesterol levels)
Antipsychotic drugs
AspirinSome Trade Names
BAYER
, ibuprofenSome Trade Names
ADVIL MOTRIN
, and many other nonprescription pain relievers (analgesics)
Vasopressin (synthetic antidiuretic hormone) and oxytocinSome Trade Names
PITOCIN
(both drugs help the body conserve fluids

bonnieh

Posted by @bonnieh, Jan 16, 2012


Hyponatremia, or low salt content in the blood, can be a serious medical problem. Salt is an important electrolyte that regulates water balance in the body. A low salt content in the blood typically means that there is too much fluid in the bloodstream, which can be placing stress on the heart and other organs. Therefore, you must adhere to the diet for hyponatremia that your physician recommends to bring your salt levels to the normal range.



Read more: http://www.livestrong.com/article/416857-diet-for-hyponatremia/#ixzz1jdXphPZl

bonnieh

Posted by @bonnieh, Jan 16, 2012

Can You Really Drink Too Much Water?

In a word, yes. Drinking too much water can lead to a condition known as water intoxication and to a related problem resulting from the dilution of sodium in the body, hyponatremia. Water intoxication is most commonly seen in infants under six months of age and sometimes in athletes. A baby can get water intoxication as a result of drinking several bottles of water a day or from drinking infant formula that has been diluted too much. Athletes can also suffer from water intoxication. Athletes sweat heavily, losing both water and electrolytes. Water intoxication and hyponatremia result when a dehydrated person drinks too much water without the accompanying electrolytes.

bonnieh

Posted by @bonnieh, Jan 16, 2012

What Happens During Water Intoxication?

When too much water enters the body's cells, the tissues swell with the excess fluid. Your cells maintain a specific concentration gradient, so excess water outside the cells (the serum) draws sodium from within the cells out into the serum in an attempt to re-establish the necessary concentration. As more water accumulates, the serum sodium concentration drops -- a condition known as hyponatremia. The other way cells try to regain the electrolyte balance is for water outside the cells to rush into the cells via osmosis. The movement of water across a semipermeable membrane from higher to lower concentration is called osmosis. Although electrolytes are more concentrated inside the cells than outside, the water outside the cells is 'more concentrated' or 'less dilute' since it contains fewer electrolytes. Both electrolytes and water move across the cell membrane in an effort to balance concentration. Theoretically, cells could swell to the point of bursting.

From the cell's point of view, water intoxication produces the same effects as would result from drowning in fresh water. Electrolyte imbalance and tissue swelling can cause an irregular heartbeat, allow fluid to enter the lungs, and may cause fluttering eyelids. Swelling puts pressure on the brain and nerves, which can cause behaviors resembling alcohol intoxication. Swelling of brain tissues can cause seizures, coma and ultimately death unless water intake is restricted and a hypertonic saline (salt) solution is administered. If treatment is given before tissue swelling causes too much cellular damage, then a complete recovery can be expected within a few days.

bonnieh

Posted by @bonnieh, Jan 16, 2012

It's Not How Much You Drink, It's How Fast You Drink It!

The kidneys of a healthy adult can process fifteen liters of water a day! You are unlikely to suffer from water intoxication, even if you drink a lot of water, as long as you drink over time as opposed to intaking an enormous volume at one time. As a general guideline, most adults need about three quarts of fluid each day. Much of that water comes from food, so 8-12 eight ounce glasses a day is a common recommended intake. You may need more water if the weather is very warm or very dry, if you are exercising, or if you are taking certain medications. The bottom line is this: it's possible to drink too much water, but unless you are running a marathon or an infant, water intoxication is a very uncommon condition.

bonnieh

Posted by @bonnieh, Jan 17, 2012

Where did people get the idea that guzzling enormous quantities of water is healthful? A few years ago Heinz Valtin, a kidney specialist from Dartmouth Medical School, decided to determine if the common advice to drink eight, eight-ounce glasses of water per day could hold up to scientific scrutiny. After scouring the peer-reviewed literature, Valtin concluded that no scientific studies support the "eight x eight" dictum (for healthy adults living in temperate climates and doing mild exercise). In fact, drinking this much or more "could be harmful, both in precipitating potentially dangerous hyponatremia and exposure to pollutants, and also in making many people feel guilty for not drinking enough," he wrote in his 2002 review for the American Journal of Physiology—Regulatory, Integrative and Comparative Physiology. And since he published his findings, Valtin says, "not a single scientific report published in a peer-reviewed publication has proven the contrary."

bonnieh

Posted by @bonnieh, Jan 17, 2012

To guard against hyponatremia you must balance your fluid intake with a well-balanced nutritional plan and indulge in less alcohol, soda, coffee and tea. Never substitute the above drinks for good clean water, fresh fruits or vegetables. Pay attention to thirst signals and establish definitive daily intakes

bonnieh

Posted by @bonnieh, Jan 17, 2012


Low Sodium Levels
A variety of factors can cause low sodium levels. Water intoxication is one such cause. This occurs when someone consumes too much water, causing an unsafe drop in electrolytes. Too much caffeine has been linked to some cases of hyponatremia. Certain diseases can also cause low sodium levels. If your sodium levels are only slightly below normal or are gradually declining, you may not experience any symptoms. Significant drops in blood sodium levels can cause disorientation, confusion or even coma. A blood test is required to determine your sodium levels.

bonnieh

Posted by @bonnieh, Jan 17, 2012


Treatment
If you have low sodium levels, follow your physician's recommendations to increase sodium intake. In some cases, your doctor will use intravenous fluids with a high amount of sodium to raise your sodium levels. In less severe cases, he may recommend certain foods or drinks. Generally, you should avoid caffeine and alcohol if you have low sodium levels because they can cause electrolyte imbalances. Certain medication can also decrease sodium levels, so discuss any medications or supplements you are taking with your doctor.


bonnieh

Posted by @bonnieh, Jan 17, 2012


A study published in "Clinical Science" in 2002 found that a high intake of caffeine causes a significant acute increase in sodium excretion. The small clinical study investigated the body's response to a 400 mg oral dose of caffeine in eight healthy males. The increase in sodium excretion suggests that caffeine may cause sodium levels to drop.


bonnieh

Posted by @bonnieh, Jan 17, 2012


High Sodium Drinks
Other than water and tea, most beverages are actually quite high in sodium. Milk and juice are among the healthier options for high-sodium drinks. Because milk can also be quite high in fat and cholesterol, opt for low-fat or skim milk. According to MayoClinic.com, one cup of low-fat milk contains about 107 mg of sodium. Adding a few spoonfuls of malted powder to that milk adds even more sodium to the drink. Check the nutrition label of various juices to find one high in sodium and relatively low in sugar. Typically, vegetable juices tend to be higher in sodium than fruit juices -- although fruit juices are still quite high in sodium. Sports drinks and soft drinks are another high-sodium beverage option. And if you are looking for a beverage to warm you up on a chilly day, consider enjoying a cup of high-sodium soup broth.



Read more: http://www.livestrong.com

bonnieh

Posted by @bonnieh, Jan 17, 2012

Most of the salt consumed in a typical diet comes from processed food, such as salted meats, nuts and cold cuts; margarine and butter; chips, hot dogs and pretzels; and canned vegetables and bottled sauces.

bonnieh

Posted by @bonnieh, Jan 17, 2012

Hassles of untreated and / or effortlessly restricted low sodium could very well be significant, perhaps debilitating in most cases. You’ll be able to aid eliminate your likelihood of developing of considerable hassles through using your treatment plan you and your medical provider style and design people who anyone. Risks of low sodium include things like:

Brain damage
Bothered equilibrium together with coordination
Seizures along with tremors
Unconsciousness and even coma

bonnieh

Posted by @bonnieh, Jan 17, 2012

Commonplace symptoms of low sodium
You will experience low sodium symptoms on a daily basis or only on one occasion throughout a despite the fact that. Every so often any of all of these low sodium symptoms is generally major:

Abdominal soreness or simply cramping
Bloating
Overall body aches
Modifications to atmosphere, identity and even behavior
Problem together with mind, considering, conversing, understanding, looking at or even writing
Dizziness
Headache
Intoxicated debt together with coordination
Malaise and also lethargy
Muscles tissue spasms
Feeling sick having or simply devoid of vomiting

bonnieh

Posted by @bonnieh, Jan 25, 2012

In recent years, hyponatremic seizures resulting from water intoxication have been reported in the United States with an increasing frequency that some have likened to an epidemic. Infants of parents living in poverty and uninformed of the risks of feeding fluids other than infant formula to their babies are particularly at risk. Young infants with vomiting and diarrhea are especially prone to developing hyponatremia if fed fluids lacking sufficient sodium, but even those who are otherwise well may develop symptomatic hyponatremia as a result of being fed excess solute-free water. Most often tap water, either in the form of supplemental feedings or overly dilute formula, has been given in excessive amounts over relatively short periods of time. Less frequently, water in other forms such as juice, soda, or tea has been implicated.

bonnieh

Posted by @bonnieh, Jan 25, 2012

The prehospital medical team was sent to a 54-year-old female who suffered from a status epilepticus. The seizures were preceded by agitation. She had no history of epileptic seizures but was well known for depression and ethylism. No arguments for alcohol withdrawal seizures were observed, but her husband mentioned that she drunk over 9 l of diet coke that day. The seizures stopped after the administration of 10 mg of diazepam intravenously. The woman was admitted with the tentative diagnosis of seizures secondary to a metabolic disorder. Laboratory analysis revealed a marked hyponatremia of 109 mmol/l with an osmolality of 232 mOsm/l, the renal function was normal. Postconvulsive rhabdomyolysis was diagnosed (creatine kinase of 2437 U/l). She recovered well after intravenous correction of the hyponatremia, forced diuresis and delirium prevention. She was under psychiatric control and remained seizure free.

bonnieh

Posted by @bonnieh, Jan 25, 2012

Hyponatremia First Aid
Victims with slurred speech, confusion, severe weakness, or loss of consciousness need medical attention immediately. Call 911 for these victims, regardless of the cause.
Heat exhaustion and dehydration can look very much like hyponatremia and are much more common. Heat stroke has a distinct set of symptoms and is a serious emergency.

Determine if the victim has been staying hydrated. If witnesses can confirm the victim has been drinking at least a pint of fluid per hour during exercise, consider the possibility of hyponatremia. In cases of rapid massive water intake -- such as college fraternity initiation -- consider the possibility of hyponatremia.

Victims of hyponatremia need salt. In minor cases -- usually just when nausea is present -- before cramps, dizziness or confusion occur, victims may feel better with salty food intake. Be very careful not to treat dehydration as hyponatremia and suggest salty foods when the victim really needs fluid. Assume any victim complaining of thirst is dehydrated.

Avoid NSAIDs like ibuprofen, aspirin, or naprosyn when concerned about hyponatremia. These pain relievers may make symptoms worse.

bonnieh

Posted by @bonnieh, Jan 25, 2012

In 1993, two infants were treated at a pediatric referral hospital in Wisconsin for hyponatremic seizures caused by water intoxication associated with bottled drinking water. This report summarizes information about these cases and a review of hospitalizations for hyponatremic seizures in this hospital during 1984-1993. Patient 1

In October 1993, a 55-day-old infant was taken by her mother to the emergency department (ED) of a local hospital for evaluation of "eye twitching." During transport, she had onset of generalized, tonic-clonic seizures. Examination at the hospital revealed periorbital and gluteal edema; her serum sodium level was 116 mEq/L (normal: 135-145 mEq/L), and metabolic acidosis was documented by blood gas analysis. Status epilepticus secondary to hyponatremia was diagnosed.

Treatment was initiated with intravenous anticonvulsants. Forty-five minutes after onset of seizures, the infant experienced respiratory depression. Following endotracheal intubation, the infant was transported to the children's hospital, where she received intravenous normal saline. Serum sodium subsequently normalized, and metabolic acidosis resolved. The infant was discharged after 5 days and recovered fully.

The infant's mother had been buying cow's milk-based infant formula and had been supplementing feedings with several ounces of bottled water for several days. She reported using bottled water as a supplement because the product was inexpensive and because she interpreted the labeling to indicate that the product had been produced specifically for infants and contained nutrients adequate for use as a feeding supplement. The mother later reported to the Food and Drug Administration (FDA) that she had substituted tap water for infant formula during the 24 hours before hospitalization.

bonnieh

Posted by @bonnieh, Jan 25, 2012

FDA warned healthcare professionals and patients of the increased risk of severe hyponatremia and seizures in patients taking desmopressin. Because of this risk, FDA has requested the following changes to the prescribing information of desmopressin:

?Intranasal desmopressin is no longer indicated for primary nocturnal enuresis (PNE)
?In patients taking desmopressin tablets for PNE, interrupt therapy during acute illness to decrease risk of electrolyte imbalance
?Instruct patients to restrict fluid intake 1 hour before and 8 hours after taking desmopressin tablets
?Use all desmopressin formulations with caution in patients at risk for water intoxication (e.g., psychogenic polydipsia, patients taking concurrent medications that may cause dry mouth)
?Intranasal desmopressin should not be used in patients with hyponatremia or with a history of hyponatremia
Inform patients and parents of children taking desmopressin about the risks of hyponatremia, the importance of limiting water intake, and the symptoms of hyponatremia

bonnieh

Posted by @bonnieh, Jan 25, 2012

About 40% of the body's sodium is contained in bone. Approximately 2-5% occurs within organs and cells and the remaining 55% is in blood plasma and other extracellular fluids. Sodium must be maintained at a specific concentration in the blood and the fluid surrounding the body's cells for the body to function properly. The body maintains a balance of sodium in the blood by matching the amount of sodium we take in with the amount excreted (put out) by the kidneys. Hyponatremia occurs when the level of sodium in the blood becomes diluted by too much water intake.

The body continually regulates its handling of sodium. When dietary sodium is too high or low, the intestines and kidneys respond to adjust concentrations to normal. During the course of a day, the intestines absorb dietary sodium while the kidneys excrete a nearly equal amount of sodium into the urine. If a low sodium diet is consumed, the intestines increase their efficiency of sodium absorption, and the kidneys reduce its release into urine.

bonnieh

Posted by @bonnieh, Jan 25, 2012

Hyponatremia can be caused by the following:
•Kidney disorders in which the kidneys have difficulty eliminating fluids.

•Disorders in organs that control the body's regulation of sodium or water. The adrenal gland secretes a hormone called aldosterone that travels to the kidney, where it causes the kidney to retain sodium by not excreting it into the urine. Addison's disease causes hyponatremia as a result of low levels of aldosterone due to damage to the adrenal gland. The hypothalamus and pituitary gland are also involved in sodium regulation by making and releasing vasopressin, known as anti-diuretic hormone, into the bloodstream. Like aldosterone, vasopressin acts in the kidney, but it causes it to reduce the amount of water released into urine. With more vasopressin production, the body conserves water, resulting in a lower concentration of plasma sodium. Certain types of cancer cells produce vasopressin, leading to hyponatremia.

•Abnormal consumption or excretion of dietary sodium or water.

•Diuretic drugs used to treat high blood pressure. These drugs make the kidneys produce more urine, which can wash away too much sodium, especially when the patient is following a low sodium diet. This is especially of concern in elderly patients, who have a reduced ability to regulate the concentrations of various nutrients in the bloodstream. Diuretic drugs that frequently cause hyponatremia include furosemide (Lasix), bumetanide (Bumex), and most commonly, the thiazides. Diuretics enhance the excretion of sodium into the urine, with the goal of correcting high blood pressure. However, too much sodium excretion can result in hyponatremia. Usually only mild hyponatremia occurs in patients taking diuretics, but when combined with a low sodium diet or with the excessive drinking of water, severe hyponatremia can develop.

•Some psychiatric disorders cause people to drink extremely large quantities of water, which can result in hyonatremia.

•Drinking excess water sometimes causes hyponatremia, because the absorption of water into the bloodstream can dilute the sodium in the blood. This cause of hyponatremia is rare, but has been found in psychotic patients who compulsively drink more than 20 liters of water per day.

•Receiving too much fluid intravenously.

•Excessive drinking of beer, which is mainly water and low in sodium, can also produce hyponatremia when combined with a poor diet.

•Maintenance of a low salt diet for many months.

•Severe and prolonged diarrhea can also cause hyponatremia. Severe diarrhea, causing the daily output of 8-10 liters of fluid from the large intestines, results in the loss of large amounts of water, sodium, and various nutrients. Some diarrheal diseases release particularly large quantities of sodium and are therefore most likely to cause hyponatremia.

•Prolonged vomiting.

•Excessive sweat loss during a race on a hot day can present a challenge to the body to conserve adequate sodium levels. Marathon running, under certain conditions, leads to hyponatremia. Races of 25-50 miles can result in the loss of great quantities (8 to 10 liters) of sweat, which contains both sodium and water. Studies show that about 30% of marathon runners experience mild hyponatremia during a race. But runners who consume only pure water during a race can develop severe hyponatremia because the drinking water dilutes the sodium in the bloodstream. Such runners may experience neurological disorders as a result of the severe hyponatremia and require emergency treatment.

•Hypothalamus and pituitary disorders.

•Certain types of cancer.
Hyponatremia is more likely to occur in people whose kidneys do not function properly, as well as in those with heart failure, cirrhosis of the liver, and Addison's disease, in which underactive adrenal glands excrete too much sodium.

bonnieh

Posted by @bonnieh, Jan 25, 2012

Because the brain is very sensitive to sodium levels, low sodium causes symptoms including confusion and lethargy. The patient may feel nauseated, and experience muscle twitching, which can progress to seizures. Eventually, severe hyponatremia can lead to coma and death.

Symptoms of moderate hyponatremia include tiredness, disorientation, headache, muscle cramps, and nausea. Severe hyponatremia can lead to seizures and coma. These neurological symptoms are thought to result from the movement of water into brain cells, causing them to swell and disrupt their functioning.

bonnieh

Posted by @bonnieh, Jan 25, 2012

Treatment and Prevention

--------------------------------------------------------------------------------
Severe hyponatremia can be treated by infusing a solution of 5% sodium chloride in water into the bloodstream. Moderate hyponatremia due to use of diuretics or an abnormal increase in vasopressin is often treated by instructions to drink less water each day. Hyponatremia due to adrenal gland insufficiency is treated with hormone injections.

When hyponatremia is severe, it is considered a medical emergency that is treated in a hospital. Very low plasma sodium levels can result in seizures and coma. The doctor will slowly increase the blood sodium levels with intravenous (IV) fluids. Additional treatment depends upon the underlying cause of hyponatremia.

If you take diuretics, make sure you have your blood sodium levels checked on a regular basis. If you are sick and symptoms include vomiting or diarrhea, follow your doctor's recommendations for replacing lost fluids with clear liquids or electrolyte replacement fluids. People who run marathons and train intensely should drink electrolyte replacement fluids to keep sodium levels balanced.

bonnieh

Posted by @bonnieh, Jan 28, 2012


The symptoms of obstructive sleep apnea are not very specific. This means that many people who snore at night or who feel tired during the day probably do not have sleep apnea. Other medical reasons for daytime sleepiness should be considered by your doctor before referral to a sleep center for diagnostic sleep tests. They include:

•Having to work excessive hours or varying shifts (nights, weekends)
•Medications (tranquilizers, sleeping pills, antihistamines beta blockers, many others)
•Alcohol abuse
•Medical conditions (such as hypothyroidism, hypercalcemia, and hyponatremia/hypernatremia)
•Self-imposed short sleep time
•Other sleep disorders, such as narcolepsy, insomnia, or restless legs syndrome
•Chronic fatigue syndrome
•Depression or dysthymia

bonnieh

Posted by @bonnieh, Jan 29, 2012

In a 3 yr period, 15 patients from a psychiatric hospital had severe hyponatremia. All but 2 of the patients were receiving antipsychotic medications, one patient was taking a non-steriodal inflamatory drug, and one patient was taking an oral hypoglycemic agent. thirteen patients were chronic schizophrenics, one had a bipolar-depressive disorder with psychotic features, and one patient had no psyc...hiatric disorder. The patients had presented seizures,change in mental status, and vegetative symptoms (neausea,vomiting, diarrhea), associated with hyponatremia and water intoxication. Exacerbation of the patients' underlying illness, psychogenic polydypsia, compulsive smoking, alcoholic cirrohsis, drug abuse, and neuoleptic and other medications are thought to be the major causes of acute hyponatremia in these patients.

bonnieh

Posted by @bonnieh, Jan 29, 2012

Risk factors for the development of hyponatremia in psychiatric inpatients.

Abstract
BACKGROUND: When inpatients who are on psychiatry services develop hyponatremia, medical consultation is usually required for evaluation and management, thus halting or delaying psychiatric treatment. Risk factors for the development of hyponatremia in this population have not been studied.

METHODS: A case-control study of psychiatric inpatients in a tertiary care facility was performed. Sixty-four patients who had a serum sodium level of less than 130 mmol/L were identified; three control subjects were chosen from the inpatient psychiatry service for each case. Risk factors investigated included medications, psychiatric diagnoses, basic demographic variables, and medical comorbidities.

RESULTS: Univariate and logistic regression analyses revealed that, in addition to diuretic use (adjusted odds ratio, 8.2; 95% confidence intervals, 2.2 to 30.8), use of fluoxetine (adjusted odds ratio, 21.4; 95% confidence interval, 5.3 to 86.9), tricyclic antidepressants (adjusted odds ratio, 4.9; 95% confidence interval, 1.6 to 15.2), and calcium antagonists (adjusted odds ratio, 4.0; 95% confidence interval, 1.1 to 14.2) were all associated with the development of hyponatremia. Important comorbidities included elevated creatinine levels, chronic obstructive pulmonary disease, hypertension, systolic blood pressure, and diabetes. Although age was significantly associated with hyponatremia in univariate analyses, it was not significant in multivariate analyses.

CONCLUSIONS: Among psychiatric patients, hyponatremia is often associated with factors other than psychogenic polydipsia, including medications and medical comorbidities. Although elderly psychiatric inpatients seem to develop hyponatremia more often than younger patients, once drugs and comorbidities are taken into account, age does not appear to be a significant risk factor for hyponatremia in this population.

bonnieh

Posted by @bonnieh, Jan 29, 2012

Hyponatraemia is known to be associated with many different drugs including diuretics, antiepileptics and psychotropic drugs. Hyponatraemia associated with use of antidepressant drugs has been described in several case reports and case series. There have also been numerous recent case reports of an association between the use of selective serotonin reuptake inhibitors (SSRIs) and hyponatraemia. In the WHO-database of adverse drug reactions, most reports of SSRI-related hyponatraemia were due to fluoxetine, paroxetine and sertraline (821, 400 and 219 reports until July 1998, respectively).Hyponatraemia is known to be a relatively frequent form of electrolyte disturbance amongst psychiatric patients. In a case-control study, Siegler and colleagues investigated risk factors for the development of hyponatraemia in psychiatric inpatients. After adjustment for potential confounders, they found that use of fluoxetine and tricyclic antidepressants (TCAs) was significantly associated with hyponatraemia, with fluoxetine showing a higher risk than TCAs. Therefore, it is not clear from this study whether fluoxetine is uniquely associated with hyponatraemia or whether other serotonin reuptake inhibitors also increase risk.

bonnieh

Posted by @bonnieh, Jan 29, 2012

Patients with hyponatremia can experience symptoms that mimic psychosis or depression. Therefore, monitoring of serum sodium levels is very important in patients who are being treated with psychotropic drugs. Also, any change in the course of the psychiatric disease may suggest the possibility of drug-induced SIADH.

bonnieh

Posted by @bonnieh, Jan 29, 2012

Hyponatremia: in some patients, a condition of low sodium (salt) levels in the blood may occur, called hyponatremia. Blood sodium levels should be monitored in those who take Trileptal for a long time, and in some cases, the doctor may recommend reducing fluid intake to keep sodium levels more balanced. Symptoms of hyponatremia include headache, nausea, and confusion.
As with any anti-seizure medication, Trileptal dosage should be tapered gradually when it is discontinued. Sudden discontinuation has a high risk of increased seizure frequency.
Trileptal can cause drowsiness and dizziness. Patients taking Trileptal should not drive or operate heavy machinery until the Trileptal’s effects are known and do not impair functioning.
Birth control: hormonal contraceptives may be less effective when taken with Trileptal.
For Pregnant or Nursing Mothers: Trileptal has not been studied in pregnant women, but studies in animals indicate that it is very likely to cause birth defects. Trileptal is similar to Tegretol, a drug which is known to cause birth defects, and therefore Trileptal is expected to have similar effects during pregnancy. Trileptal is passed into breast milk, and nursing while taking Trileptal is not advised.

bonnieh

Posted by @bonnieh, Jan 29, 2012

Many psychiatric patients have polydipsia and polyuria without identifiable underlying medical causes. Hyponatremia develops in some polydipsic patients and can progress to water intoxication with such symptoms as confusion, lethargy, psychosis, and seizures or death. This syndrome is sometimes called "compulsive water drinking," "psychogenic polydipsia," and "self-induced water intoxication." Although the underlying pathophysiology of the syndrome is unclear, several factors have been implicated in producing polydipsia and symptomatic hyponatremia. These include a possible hypothalamic defect, the syndrome of inappropriate secretion of ADH (SIADH), and neuroleptic medication. Evaluation of psychiatric patients with polydipsia includes a search for other medical causes of polydipsia, polyuria, hyponatremia, and SIADH.

bonnieh

Posted by @bonnieh, Jan 29, 2012

Drug-induced hyponatraemia is commonly associated with diuretics, selective serotonin reuptake inhibitors and antiepileptics. With increasing polypharmacy and an ageing population, the prevalence of drug-induced hyponatraemia is likely to increase. Most patients with drug-induced hyponatraemia are asymptomatic and the diagnosis is made incidentally following routine blood tests. Mild cases may be managed either by stopping the drug or by careful observation if the drug is considered essential. More severe hyponatraemia may require fluid restriction in the short term as well as withdrawal of the causal drug. Referral may be required for patients with acute illness and for those with severe and/or refractory hyponatraemia.

bonnieh

Posted by @bonnieh, Jan 29, 2012

Although drugs are a common cause of hyponatraemia, other causes should be considered. Assessing the patient's fluid status and plasma osmolality can help in finding the cause. As hyponatraemia is often associated with fluid retention (dilutional hyponatraemia) the osmolality is usually reduced, however other causes may be associated with normal or increased osmolality.

In normovolaemic patients the syndrome of inappropriate secretion of antidiuretic hormone is the most frequent mechanism for hyponatraemia. Drugs are often responsible for this syndrome, but may cause hyponatraemia in other ways. In Australia, drug-related hyponatraemia is most commonly reported in association with diuretics and selective serotonin reuptake inhibitors (SSRIs), but other drugs can be implicated.

With mild drug-related hyponatraemia the drug should be stopped where possible, but if the drug is essential continue it while monitoring the hyponatraemia. When hyponatraemia is more marked short-term fluid restriction and medication withdrawal may be required. In other circumstances referral is advisable.

bonnieh

Posted by @bonnieh, Jan 30, 2012

Psychiatric medications that can cause hyponatremia )-:

Carbamazepine

SSRIs

Thorazine

Depakote

Trileptal

Cogentin

Benadryl

bonnieh

Posted by @bonnieh, Jan 30, 2012

Other culprits that decrease serum sodium )-:

Thiazide diuretics (hydrochlorothiazide = HCTZ)

Vasopressin analogs (desmopressin = DDAVP, which is used to treat nocturnal enuresis)

Ectasy



Psychiatric medication that dilutes urine, increasing serum sodium (-:
Lithium - directly impairs kidney’s response to ADH. HOWEVER, DUE TO LITHIUM’S POTENTIAL TOXICITY TO KIDNEY, IT IS NOT A PREFERRED DRUG FOR TREATING SIADH





Medications that ameliorate SIADH by diluting urine, increasing serum sodium (-:

Loop diuretics – Furosemide (LASIX) prevent the urine from becoming concentrated (prevent sodium from being excreted)

Demeclocycline (a tetracycline antibiotic)

bonnieh

Posted by @bonnieh, Jan 30, 2012

[Hyponatremia associated with psychotropic drugs: a side effect to consider].

The use of psychotropic drugs has been frequently associated with hyponatremia, which is defined as a serum sodium level of less than 136 mEq/l. The main cause in the psychiatric population is the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). Age, female sex and polypharmacy are risk factors for hyponatremia. In psychiatric patients, the symptomatology caused by hyponatremia may be confused with the mental illness itself, delaying its diagnosis. Early symptoms are nausea, vomits, anorexia, headaches, weakness, irritability, agitation, lethargy, confusion and cramps. The risk of hyponatremia increases with the use of several psychiatric drugs associated with SIADH. This complication is more often diagnosed at the first weeks of treatment. The first step of treatment is to determine the real level of hypoosmolality by measuring plasmatic osmolality. A urinary osmolality equal to or higher than 100 mOsm/kg combined with an elevated concentration of urinary sodium may lead to the diagnosis of SIADH. The main treatment for drug-caused hyponatremia is medication monitoring and normalization of extracellular liquid volume. In most cases this is achieved by discontinuing medication and restricting fluid intake.

bonnieh

Posted by @bonnieh, Jan 30, 2012

Polydipsia is a non-medical symptom in which the patient displays excessive thirst.[1] The word derives from the Greek ?????????,[2] which is derived from ????? (polys, "much, many") + ???? (dipsa, "thirst"). An etymologically related term is dipsomaniac, meaning an alcoholic.

bonnieh

Posted by @bonnieh, Jan 30, 2012

Polydipsia in psychiatric subsets
Psychogenic polydipsia is an excessive water intake seen in some patients with mental illnesses such as schizophrenia, and/or the developmentally disabled. It should be taken very seriously, as the amount of water ingested exceeds the amount that can be excreted by the kidneys, and can on rare occasions be life-threatening as the body's serum sodium level is diluted to an extent that seizures and cardiac arrest can occur.
While psychogenic polydipsia is generally not found outside the population of serious mental disorders, there is some anecdotal evidence of a milder form (typically called 'habit polydipsia' or 'habit drinking') that can be found in the absence of psychosis or other mental conditions. The excessive levels of fluid intake may result in a false diagnosis of diabetes insipidus, since the chronic ingestion of excessive water can produce diagnostic results that closely mimic those of mild diabetes insipidus. As discussed in the entry on diabetes insipidus, "Habit drinking (in its severest form termed psychogenic polydipsia) is the most common imitator of diabetes insipidus at all ages. While many adult cases in the medical literature are associated with mental disorders, most patients with habit polydipsia have no other detectable disease. The distinction is made during the water deprivation test, as some degree of urinary concentration above isosmolar is usually obtained before the patient becomes dehydrated." However, prior to a water deprivation test, consideration should be given to a psychiatric consult to see whether it is possible to rule out psychogenic polydipsia or habit polydipsia

bonnieh

Posted by @bonnieh, Jan 30, 2012

Primary polydipsia or psychogenic polydipsia is a special form of polydipsia. It is usually associated with a patient's increasing fluid intake due to the sensation of having a dry mouth.
When the term "psychogenic polydipsia" is used, it implies that the condition is caused by mental disorders. However, the dry mouth is often due to phenothiazine medications used in some mental disorders, rather than the underlying condition.
Some forms of primary polydipsia are explicitly characterized as non-psychogenic.
PathophysiologyThe patient drinks large amounts of water, which dilutes the extracellular fluid, decreasing its osmotic pressure. The body responds to this by decreasing the level of vasopressin (antidiuretic hormone), with a resultant increased production of urine (polyuria). This urine will have a low electrolyte concentration.
Clinical presentationPatients have been known to seek fluids from any source possible.
In extreme episodes, the patient's kidneys will be unable to deal with the fluid overload, and weight gain will be noted.
Primary polydipsia can be life threatening as serum sodium is diluted to an extent that seizures and cardiac arrest can occur.
Diagnostic workupThe test of choice to distinguish primary polydipsia from diabetes insipidus is by fluid restriction. In primary polydipsia, the urine osmolality should increase and stabilize at above 280 Osm/kg.[4] Stabilization in this test means, more specifically, when the hourly increase in osmolality is less than 30 Osm/kg per hour for at least 3 hours.[4] A stabilization at an osmolality of less than 280 Osm/kg indicates diabetes insipidus.
TreatmentIf the patient is institutionalised, close monitoring by staff is necessary to control fluid intake.
In treatment-resistant polydipsic psychiatric patients, regulation in the inpatient milieu can be accomplished by use of a weight-water protocol. First, baseline weights must be established and correlated to serum sodium levels. Weight will normally fluctuate during the day, but as the water intake of the polydipsic goes up, the weight will naturally rise. The physician can order a stepped series of interventions as the weight rises. The correlation must be individualized with attention paid to the patient's normal weight and fluctuations, diet, comorbid disorders (such as a seizure disorder) and urinary system functioning. Progressive steps might include redirection, room restriction, and increasing levels of physical restraint with monitoring. Such plans should also progressive increases in monitoring, as well as a level at which a serum sodium level is drawn.
It is important to note that the majority of psychotropic drugs (and a good many of other classes) can cause dry mouth, but this is not to be confused with true polydipsia in which a dangerous drop in serum sodium will be seen.
Primary polydipsia often leads to institutionalization as it can be very difficult to manage outside the inpatient setting.
Patient profilesPsychogenic polydipsia is a type of polydypsia described in patients with mental illnesses and/or the developmentally disabled. It is present in a subset of people with schizophrenia. These patients, most often with a long history of illness, exhibit enlarged ventricles and shrunken cortex on MRI, making the physiological mechanism difficult to isolate from the psychogenic.
While psychogenic polydipsia is usually not seen outside the population of those with serious mental disorders, it may occasionally be found among others in the absence of psychosis, although there is no extant research to document this other than anecdotal observations. Such persons typically prefer to possess bottled water that is ice cold, consume water and other fluids at excessive levels, and may be falsely diagnosed as suffering from diabetes insipidus, since the chronic ingestion of excessive water can produce symptoms and diagnostic results that mimic mild diabetes insipidus.

bonnieh

Posted by @bonnieh, Jan 30, 2012

Polydipsia and hyponatremia in psychiatric patients.

Many psychiatric patients have polydipsia and polyuria without identifiable underlying medical causes. Hyponatremia develops in some polydipsic patients and can progress to water intoxication with such symptoms as confusion, lethargy, psychosis, and seizures or death. This syndrome is sometimes called "compulsive water drinking," "psychogenic polydipsia," and "self-induced water intoxication." Although the underlying pathophysiology of the syndrome is unclear, several factors have been implicated in producing polydipsia and symptomatic hyponatremia. These include a possible hypothalamic defect, the syndrome of inappropriate secretion of ADH (SIADH), and neuroleptic medication. Evaluation of psychiatric patients with polydipsia includes a search for other medical causes of polydipsia, polyuria, hyponatremia, and SIADH. Treatment modalities currently available include fluid restriction and medications.

bonnieh

Posted by @bonnieh, Jan 30, 2012

Psychiatric patients, particularly those with schizophrenia, often have abnormalities in water balance. As an example, one study of 239 hospitalized patients found that 6.6 percent had a history compatible with compulsive water drinking and that one-half of these had intermittent symptoms of hyponatremia due to transient water retention. However, a higher percentage of patients may have milder defects in water homeostasis.

ABNORMALITIES IN WATER BALANCE
Evaluation of psychotic patients has revealed that a variety of defects in water handling can occur, affecting thirst, the release of antidiuretic hormone (ADH), and the renal response to ADH. Depending upon which abnormality is present, the patient may present with polydipsia and polyuria and/or hyponatremia.
Primary polydipsia — Many chronically psychotic patients have a moderate to marked increase in water intake. This may be manifested clinically by exaggerated weight gain during the day (2.2 percent versus 0.6 percent in normal controls in one study) that is associated with a transient reduction in the plasma sodium concentration. (Accurate 24-hour urine collections are often difficult to obtain in psychotic patients; as a result, the mean daytime weight gain is used as an index of increased intake.)
It is presumed that a central defect in thirst regulation plays an important role in the pathogenesis of polydipsia. In some cases, for example, the osmotic threshold for thirst is reduced below the threshold for the release of antidiuretic hormone (ADH). These patients will continue to drink until the plasma tonicity is less than the threshold level. (The plasma tonicity refers to that portion of the total plasma osmolality that generates an osmotic pressure; in most cases, tonicity is determined by the concentration of the nonurea solutes.) This may be difficult to achieve, however, since ADH secretion will be suppressed by the fall in plasma tonicity, resulting in rapid excretion of the excess water and continued stimulation of thirst.
The osmotic regulation of thirst is different from that in normal subjects in whom the thirst threshold is a roughly equal to or a few mosmol/kg higher than the threshold for ADH.

bonnieh

Posted by @bonnieh, Jan 30, 2012

Over the past ten years, the authors have treated more than 100 patients with the polydipsia-hyponatremia syndrome. The authors discuss their and others' experience with drugs that help and hinder patients suffering from dilutional hyponatremia. They review current key articles from the polydipsia-hyponatremia syndrome literature including articles identified via Medline search 1985-94.

RESULTS: Schizophrenics with the polydipsia-hyponatremia syndrome most commonly present with polydipsia, polyuria, urinary incontinence, cognitive, affective, and behavioral changes, seizures, or coma. Quantitating polydipsia, hyponatremia, and diurnal changes in body weight facilitate therapeutic interventions. Treatment include patient and caregiver education, drug therapies to better treat psychosis and better treat osmotic dysregulation, behavioral interventions to interdict polydipsia, and diurnal weight monitoring.

CONCLUSIONS: Once recognized, acute, subacute, and chronic complications of the polydipsia-hyponatremia syndrome are readily treatable. Besides treating the patient, consultation/liaison psychiatrists can teach their medical colleagues about this syndrome. In so doing, they will enhance the quality of their patients' lives and help the internist and surgeon feel more comfortable when working with schizophrenics.

bonnieh

Posted by @bonnieh, Jan 30, 2012

Tobacco Smoking and Hyponatremia in Psychiatric Patients:

In a study of ten compulsive drinkers we found that episodes of hyponatremia developed only in heavy smokers. We have previously looked at this question of heavy smokers and hyponatremia and polydipsia. In our study, we found that most of the patients who presented with hyponatremia and severe neurological dysfunction were heavy smokers. ...However, when compared with normonatremic schizophrenics, the rate of smoking was not different.

Many studies concerning hyponatremia and schizophrenia do show that these patients may have inappropriate release of antidiuretic hormone (ADH) associated with their polydipsia. Factors that cause this release of ADH remain uncertain.

bonnieh

Posted by @bonnieh, Feb 5, 2012

Tegretol
All medicines may cause side effects, but many people have no, or minor, side effects. Check with your doctor if any of these most COMMON side effects persist or become bothersome when using Tegretol:

Dizziness; drowsiness; dry mouth; nausea; unsteadiness; vomiting.

Seek medical attention right away if any of these SEVERE side effects occur when using Tegretol:
Severe allergic reactions (rash; hives; itching; difficulty breathing; tightness in the chest; swelling of the mouth, face, lips, or tongue); black, tarry, or bloody stools; calf pain, swelling, or tenderness; change in the amount of urine produced; chest pain; confusion; dark urine; decreased coordination; fainting; fast, slow, or irregular heartbeat; fever, chills, or sore throat; hallucinations; joint pain; light-headedness; loss of appetite; menstrual changes; new or worsening mental or mood changes (eg, aggression, agitation, anger, anxiety, depression, irritability, restlessness); pain, tenderness, or unusual swelling in the neck, groin, or under the arms; red or purple spots on your body; red, swollen, blistered, or peeling skin; severe or persistent dizziness or headache; severe or persistent nausea or vomiting; shortness of breath; speech problems; stomach pain; sudden, unusual weight gain; suicidal thoughts or actions; swelling of the hands, ankles, or feet; swollen lymph nodes; trouble sleeping; ulcers or sores in the mouth; uncontrolled muscle movements; unusual bruising or bleeding (eg, bleeding gums, nosebleeds); unusual tiredness or weakness; vision or eye problems; yellowing of the skin or eyes.

This is not a complete list of all side effects that may occur. If you have questions about side effects, contact your health care provider. Call your doctor for medical advice about side effects.

bonnieh

Posted by @bonnieh, Feb 5, 2012

Metabolic Changes when dealing with Risperdal:
Atypical antipsychotic drugs have been associated with metabolic changes that may increase cardiovascular/cerebrovascular risk. These metabolic changes include hyperglycemia, dyslipidemia, and body weight gain. While all of the drugs in the class have been shown to produce some metabolic changes, each drug has its own specific risk profile.

Hyperglycemia and Diabetes Mellitus

Hyperglycemia and diabetes mellitus, in some cases extreme and associated with ketoacidosis or hyperosmolar coma or death, have been reported in patients treated with atypical antipsychotics including Risperdal®. Assessment of the relationship between atypical antipsychotic use and glucose abnormalities is complicated by the possibility of an increased background risk of diabetes mellitus in patients with schizophrenia and the increasing incidence of diabetes mellitus in the general population. Given these confounders, the relationship between atypical antipsychotic use and hyperglycemia-related adverse events is not completely understood. However, epidemiological studies suggest an increased risk of treatment-emergent hyperglycemia-related adverse events in patients treated with the atypical antipsychotics. Precise risk estimates for hyperglycemia-related adverse events in patients treated with atypical antipsychotics are not available.

Patients with an established diagnosis of diabetes mellitus who are started on atypical antipsychotics, including Risperdal®, should be monitored regularly for worsening of glucose control. Patients with risk factors for diabetes mellitus (e.g., obesity, family history of diabetes) who are starting treatment with atypical antipsychotics, including Risperdal®, should undergo fasting blood glucose testing at the beginning of treatment and periodically during treatment. Any patient treated with atypical antipsychotics, including Risperdal®, should be monitored for symptoms of hyperglycemia including polydipsia, polyuria, polyphagia, and weakness. Patients who develop symptoms of hyperglycemia during treatment with atypical antipsychotics, including Risperdal®, should undergo fasting blood glucose testing. In some cases, hyperglycemia has resolved when the atypical antipsychotic, including Risperdal®, was discontinued; however, some patients required continuation of anti-diabetic treatment despite discontinuation of Risperdal®.

bonnieh

Posted by @bonnieh, Feb 5, 2012

Antipsychotic-Induced Hyponatraemia: A Systematic Review of the Published Evidence

Supplemental Author MaterialAbstract: Hyponatraemia is known to occur as a rare but clinically important adverse reaction to treatment with different psychotropic drugs, including selective serotonin reuptake inhibitors and antiepileptic drugs. In past decades, reports have been published that describe the development of hyponatraemia in association with antipsychotic drug treatment. Our objective was to systematically review the available evidence on antipsychotic-induced hyponatraemia, focussing on patient characteristics, drug dosage, polydipsia and the syndrome of inappropriate secretion of antidiuretic hormone (SIADH).

A search was carried out in the MEDLINE and EMBASE databases from January 1966 to 11 April 2009. Inclusion criteria were hyponatraemia (serum sodium level <136?mmol/L) occurring after the start of treatment with an antipsychotic drug; and that the hyponatraemia potentially occurred as an adverse reaction to antipsychotic drug treatment in accordance with the WHO definition. Articles in languages other than English, Dutch, German, French and Spanish were excluded. Information on patient characteristics, medical and diagnostic data, pharmacological treatment, drug dechallenge and drug rechallenge were extracted from the publications whenever available. A causality assessment was performed on all case reports using Naranjo's adverse drug reaction probability scale. Correlational analysis was performed to assess correlations between antipsychotic drug dosage and both serum sodium level and time to onset of hyponatraemia.

We included four studies and 91 publications containing case reports and case series; no randomized controlled studies were identified. Data from the identified case reports were further analysed. The mean age of the patients was 46 years; 57% were male. The diagnosis was schizophrenia in 70% of the cases. A history of polydipsia was diagnosed as positive in 67% of the cases and negative in 23% of the cases. Polydipsia occurred in the remaining 10% of cases, although it was reported to be drug-induced (i.e. a severe increase in water intake was observed in relation to treatment with the suspected drug). Analysis of the case reports using the adverse drug reaction probability scale indicated possible causality in most cases (80%), probable causality in a significant amount of cases (19%) and unlikely causality in one case (1%). Overall correlational analysis yielded no significant correlations between defined daily dose-equivalent dosages and serum sodium or time to onset of hyponatraemia.

The incidence of hyponatraemia induced by antipsychotics may be much higher than is currently thought. Both the newer atypical antipsychotics and the older drugs have been associated with the development of hyponatraemia. Physicians, psychiatrists and other healthcare workers should be aware of the possibility of hyponatraemia associated with the use of antipsychotics. Further studies are required to establish the risks of and risk factors associated with antipsychotic-induced hyponatraemia.

bonnieh

Posted by @bonnieh, Feb 5, 2012

Hyponatraemia as an Adverse Drug Reaction of Antipsychotic Drugs: A Case-Control Study in VigiBase

Abstract: Background: Hyponatraemia due to antipsychotic use is a potentially serious problem; however, it is not known whether it is an adverse drug reaction (ADR) to antipsychotic use or is due to the underlying psychiatric disease.

Objective: To estimate the strength of the association between antipsychotics and hyponatraemia or syndrome of inappropriate antidiuretic hormone secretion (SIADH), using information reported to the WHO Collaborating Centre for International Drug Monitoring, the Uppsala Monitoring Centre (UMC).

Setting: The WHO global individual case safety report database system (VigiBase) maintained by the UMC.

Study Design: Case-control study, with cases being reports of hyponatraemia/SIADH, and controls being reports of other ADRs. Each case was sampled with ten controls sequencing in time from the date the corresponding case was entered into the database. The potential contribution of the chemical structures and receptor affinity (dopaminergic and/or serotonergic) of the antipsychotics was studied, as was the influence of concomitant use of other medications known to cause hyponatraemia.

Main Outcome Measures: The strength of the association between antipsychotic use and hyponatraemia in comparison with other drugs was expressed as reporting odds ratio (ROR), a measure of disproportionality, with corresponding 95% CIs, adjusted for age, sex and concomitant medication associated with hyponatraemia. In addition, stratification by the presence or absence of concomitant medication was performed.

Results: Up to August 2008, 3?881?518 suspected ADRs were reported and filed in VigiBase, with 912 reports on hyponatraemia related to antipsychotics. The adjusted ROR for the association between antipsychotic use and hyponatraemia was 1.58 (95% CI 1.46, 1.70). The adjusted RORs did not vary for the different chemical structures or dopamine D2 and serotonin 5-HT2A receptor affinity profiles. The ROR was 3.00 (95% CI 2.65, 3.39) for the association between hyponatraemia and antipsychotic use in the absence of concomitant medication associated with hyponatraemia, and 1.16 (95% CI 1.06, 1.28) in the presence of concomitant medication associated with hyponatraemia.

Conclusions: Antipsychotic use may be associated with reporting of hyponatraemia. Moreover, the concomitant use of medication associated with hyponatraemia potentially leads to under-reporting of antipsychotic-associated hyponatraemia. We advise testing patients whose psychiatric and/or physical condition deteriorates while on antipsychotics for hyponatraemia.

bonnieh

Posted by @bonnieh, Feb 5, 2012

Drug-Induced SIADH
Initially, pharmacologic agents that had antidiuretic action were prescribed to treat patients with diabetes insipidus (DI). Later on, numerous reports documented serious adverse effects, such as water retention and dilutional hyponatremia, associated with these drugs.
The proposed mechanism by which a drug interferes with the normal secretion and action of ADH depends on the drug.Drugs that stimulate the release of ADH from the posterior pituitary gland include nicotine, phenothiazines, and tricyclics. Some drugs increase or potentiate the renal action of ADH. They include desmopressin, oxytocin, and prostaglandin synthesis inhibitors. Drugs that cause SIADH by means of mixed or uncertain mechanism of action include chlorpropamide, carbamazepine, cyclophosphamide, and vincristine.
In 1994, researchers reported the first case suggesting a cause-effect relationship between omeprazole and SIADH. However, the mechanism of omeprazole-induced SIADH needs to be established.
Ecstasy, or 3,4 methylene dioxymethamphetamine (MDMA), a powerful derivative of amphetamine that is popular among adolescents, can cause SIADH. However, the mechanism of MDMA-induced SIADH is not well understood.
SIADH induced by angiotensin-converting enzyme (ACE) inhibitors (eg, lisinopril) is a rare but possible adverse effect of this category of drugs.The SIADH-type of dilutional hyponatremia induced by ACE inhibitors may be mediated by the potentiation of the action of plasma renin, which results in increased levels of brain angiotensin. This, in turn, results in the release of AVP from the hypothalamus and an increase in thirst.
A review article in Drugs & Aging provides an in-depth discussion of the mechanisms of action by which drugs may induce SIADH.

bonnieh

Posted by @bonnieh, Feb 6, 2012

Psychotropic Drugs
It is estimated that psychotropic drugs are administered to approximately 50% of institutionalized older patients.Some of the older antipsychotic drugs, such as fluphenazine, thiothixene, and phenothiazine, and the tricyclic antidepressants (eg, amitriptyline) can cause hyponatremia with characteristics of SIADH.
A systematic review of reported cases was conducted to evaluate the relationship between hyponatremia and SIADH with the use of selective serotonin reuptake inhibitors (SSRIs), including fluoxetine, fluvoxamine, paroxetine, and sertraline. According to the study, fluoxetine is the SSRI most commonly reported to cause hyponatremia and SIADH. However, the mechanism of action responsible for SSRI-induced SIADH is not known.
According to the 30 published reports of hyponatremia and SIADH associated with SSRIs, age ? 65 years may be a risk factor for hyponatremia and SIADH associated with SSRIs.More than 50% of these patients developed hyponatremia within 13 days. The hyponatremia was reversible within 2-28 days after the SSRI was discontinued.
Patients with hyponatremia can experience symptoms that mimic psychosis or depression. Therefore, monitoring of serum sodium levels is very important in patients who are being treated with psychotropic drugs. Also, any change in the course of the psychiatric disease may suggest the possibility of drug-induced SIADH.

bonnieh

Posted by @bonnieh, Feb 6, 2012

Antipsychotic-Induced Hyponatremia: Case Report and Literature Review

Abstract: We report a case of hyponatremia in a patient that occurred 3 days after initiation of treatment with aripiprazole. The patient was a 50-year-old man admitted to an inpatient psychiatric unit for exacerbation of schizophrenia. He was started on aripiprazole and developed hyponatremia that resolved when the medication was stopped. We postulate that the hyponatremia was due to an aripiprazole-induced syndrome of inappropriate secretion of antidiuretic hormone. There have been numerous case reports in the literature of hyponatremia in the literature associated with atypical antipsychotics. We caution clinicians to be aware that the potential hyponatremic-inducing effects of atypical antipsychotics can occur rapidly after initiation of the medications.

bonnieh

Posted by @bonnieh, Feb 6, 2012

A variety of factors can contribute to the development of hyponatremia in patients with cirrhosis. The most important factor is systemic vasodilation, which leads to activation of endogenous vasoconstrictors including antidiuretic hormone (ADH); ADH promotes the water retention that is responsible for the fall in serum sodium.
Systemic vasodilation — Systemic vasodilation plays a central role in the pathogenesis of hyponatremia in patients with cirrhosis and ascites. These patients usually have a marked reduction in systemic vascular resistance (SVR) and in mean arterial pressure and an increase in cardiac output . The vascular territory in which the reduced SVR is most obvious is the splanchnic circulation.
The presence of vasodilation in other vascular territories is less obvious and the subject of controversy. As an example, the factors that cause splanchnic vasodilatation may have a biphasic effect on the renal circulation. Early in the course of the disease — stable cirrhosis without ascites — the dilating substances also may influence the renal vasculature and the glomerular filtration rate may be greater than normal (150 versus 105 mL/min in one study) at this stage. With more severe disease, the splanchnic vasodilatation becomes more marked, resulting in a fall in mean arterial pressure and decreased renal perfusion, leading in some patients to the hepatorenal syndrome.
The precise mechanisms of vasodilation in cirrhosis have become better understood, with increased generation of nitric oxide and prostaglandins appearing to play an important role. Nitric oxide production may be stimulated by absorbed endotoxin from the gastrointestinal tract, which is less efficiently cleared due to portal-systemic shunting and decreased reticuloendothelial cell function in cirrhosis.

bonnieh

Posted by @bonnieh, Feb 6, 2012

Hyponatremia in cirrhosis: pathogenesis, clinical significance, and management.

Abstract
Hyponatremia is a frequent complication of advanced cirrhosis related to an impairment in the renal capacity to eliminate solute-free water that causes a retention of water that is disproportionate to the retention of sodium, thus causing a reduction in serum sodium concentration and hypo-osmolality. The main pathogenic factor responsible for hyponatremia is a nonosmotic hypersecretion of arginine vasopressin (or antidiuretic hormone) from the neurohypophysis related to circulatory dysfunction. Hyponatremia in cirrhosis is associated with increased morbidity and mortality. There is evidence suggesting that hyponatremia may affect brain function and predispose to hepatic encephalopathy. Hyponatremia also represents a risk factor for liver transplantation as it is associated with increased frequency of complications and impaired short-term survival after transplantation. The current standard of care based on fluid restriction is unsatisfactory. Currently, a new family of drugs, known as vaptans, which act by antagonizing specifically the effects of arginine vasopressin on the V2 receptors located in the kidney tubules, is being evaluated for their role in the management of hyponatremia. The short-term treatment with vaptans is associated with a marked increase in renal solute-free water excretion and improvement of hyponatremia. Long-term administration of vaptans seems to be effective in maintaining the improvement of serum sodium concentration, but the available information is still limited. Treatment with vaptans represents a novel approach to improving serum sodium concentration in cirrhosis.

bonnieh

Posted by @bonnieh, Feb 6, 2012

Water retention and cirrhosis
The pathophysiology of hyponatremia in cirrhosis is multifactorial. On the simplest level, vasopressin is elevated in cirrhosis because metabolic clearance by the liver is impaired, correlating with disease severity.

In patients who have cirrhosis with ascites, liver and kidney function both are diminished. In addition, urine clearance after a water load provocation is reduced proportionally to the level of end-organ disease. Vasopressin also plays a role in water retention and is elevated along with norepinephrine, renin, and aldosterone in patients in whom water load excretion is significantly impaired. This process represents a nonosmotic stimulus for vasopressin secretion.

bonnieh

Posted by @bonnieh, Feb 8, 2012


Cirrhosis of the liver commonly leads to a state of chronic hypervolemic hyponatremia. Profound exacerbation of the hyponatremic state may occur in patients with decompensated cirrhosis in conjunction with acute stressors such as infection or binge alcohol ingestion.
A 47 year old man with a history of alcoholic cirrhosis presented to the hospital with symptomatic profound hyponatremia (serum sodium concentration of 105 meq/L) due to a recent infection and binge drinking. The patient was treated with antibiotics, diuretics and hypertonic saline and was placed on a fluid restricted diet. The serum sodium level corrected slowly over four days with symptomatic improvement occurring after two days. A brief discussion of the symptoms and treatment of acute and chronic hyponatremia in the setting of cirrhosis is included.
In patients with cirrhosis, it is important to recognize the symptoms of hyponatremia, identify and treat any exacerbating conditions early in their course, and correct the serum sodium concentration slowly with frequent monitoring.

bonnieh

Posted by @bonnieh, Feb 9, 2012

Hyponatremia is a condition that occurs when the level of sodium in your blood is abnormally low.
Sodium is an electrolyte, and it helps regulate the amount of water that's in and around your cells. In hyponatremia, one or more factors — ranging from an underlying medical condition to drinking too much water during endurance sports — causes the sodium in your body to become diluted. When this happens, your body's water levels rise, and your cells begin to swell. This swelling can cause many health problems, from mild to severe.
Hyponatremia treatment is aimed at resolving the underlying condition. Depending on the cause of hyponatremia, you may simply need to cut back on how much you drink. In other cases of hyponatremia, you may need intravenous fluids and medications.

bonnieh

Posted by @bonnieh, Feb 10, 2012

Cardiac conduction defects associated with hyponatremia.

Abstract
Cardiac conduction defects have not been previously described in association with hyponatremia, although in patients with congestive heart failure the frequency of ventricular premature beats was found to correlate to the severity of hyponatremia. We describe three patients with second-degree or complete atrioventricular (AV) block which occurred during or shortly after an episode of severe hyponatremia. The first had thiazide-induced hyponatremia while on amiodarone. In the second, definite etiology for hyponatremia which was associated with longstanding polydipsia could not be established. The third had ischemic heart disease and intermittent conversion of his first-degree to second-degree AV block while hyponatremic after diuretics use. Although it is usually difficult to single out hyponatremia as the cause of conduction defects which usually occur in the presence of cardiac disease, potent medications or other electrolyte abnormalities, we suggest that hyponatremia may play a role in the pathogenesis of conduction defects in the diseased heart.

bonnieh

Posted by @bonnieh, Feb 10, 2012

Serum sodium concentration and serum osmolarity normally are maintained under precise control by homeostatic mechanisms involving stimulation of thirst, secretion of antidiuretic hormone (ADH), and renal handling of filtered sodium. Clinically significant hyponatremia is relatively uncommon and is nonspecific in its presentation; therefore, the physician must consider the diagnosis in patients presenting with vague constitutional symptoms or with altered level of consciousness. Irreparable harm can befall the patient when abnormal serum sodium levels are corrected too quickly or too slowly. The physician must have a thorough understanding of the pathophysiology of hyponatremia to initiate safe and effective corrective therapy. The patient's fluid status must be accurately assessed upon presentation, as it guides the approach to correction.

Hypovolemic hyponatremia
Total body water (TBW) decreases; total body sodium (Na+) decreases to a greater extent. The extracellular fluid (ECF) volume is decreased.

Euvolemic hyponatremia
TBW increases while total sodium remains normal. The ECF volume is increased minimally to moderately but without the presence of edema.

Hypervolemic hyponatremia
Total body sodium increases, and TBW increases to a greater extent. The ECF is increased markedly, with the presence of edema.

Redistributive hyponatremia
Water shifts from the intracellular to the extracellular compartment, with a resultant dilution of sodium. The TBW and total body sodium are unchanged. This condition occurs with hyperglycemia or administration of mannitol.

Pseudohyponatremia
The aqueous phase is diluted by excessive proteins or lipids. The TBW and total body sodium are unchanged. This condition is seen with hypertriglyceridemia and multiple myeloma.

bonnieh

Posted by @bonnieh, Feb 10, 2012

Hyponatremia due to heart failure (HF) and almost all other causes results from an inability to excrete ingested water. This problem in HF is largely related to the associated fall in cardiac output and systemic blood pressure, which stimulate secretion of the three "hypovolemic" hormones — renin (with a subsequent increase in angiotensin II formation), antidiuretic hormone (ADH), and norepinephrine. Although edematous patients with HF have increased plasma and extracellular fluid volumes, they are effectively volume depleted, since the low cardiac output decreases the pressure perfusing the baroreceptors in the carotid sinus and the renal afferent arteriole.

The degree of neurohumoral activation is generally related to the severity of cardiac dysfunction, as assessed by left ventricular ejection fraction or functional class. The neurohumoral changes limit both sodium and water excretion in an attempt to return perfusion pressure to normal. ADH release directly enhances water reabsorption in the collecting tubules, whereas angiotensin II and norepinephrine limit distal water delivery (and thereby water excretion) by lowering the glomerular filtration rate (due to a marked reduction in renal perfusion) and by increasing proximal sodium and water reabsorption. In addition, both the low cardiac output and high angiotensin II levels are also potent stimuli to thirst, leading to enhanced water intake.

bonnieh

Posted by @bonnieh, Feb 10, 2012

One effect of the correlation between the degree of neurohumoral activation and the severity of cardiac dysfunction is that both ADH release and the associated reduction in the serum sodium concentration parallel the severity of the heart failure. This relationship has prognostic importance, since patient survival is significantly reduced (in comparison to normonatremic patients) once the serum sodium concentration falls below 137 meq/L in patients, and may also be associated with an adverse prognosis following an acute myocardial infarction. A similar inverse correlation exists between patient survival and the degree of elevation in serum norepinephrine levels.

A serum sodium concentration below 125 meq/L represents near end-stage disease. At this time, hyperkalemia is also a frequent finding. Distal sodium and water delivery are so low in advanced cardiac disease that potassium excretion (which is primarily derived from distal potassium secretion) falls below the level of intake.

bonnieh

Posted by @bonnieh, Feb 10, 2012

How is hyponatremia (low blood sodium) treated?

Mild chronic hyponatremia may not require treatment other than adjustments in diet, lifestyle, or medications. For severe or acute hyponatremia, treatment typically involves the intravenous administration of fluids and electrolytes. In this case medications are often needed that treat the underlying cause of the hyponatremia as well as medications to manage the accompanying symptoms.

Hyponatremia At A Glance

Hyponatremia refers to a low level of sodium in the blood.

Hyponatremia may result from excess fluid in the body relative to a normal amount of sodium, or it may be due to a loss of sodium and body fluid.

Symptoms are nonspecific and can include mental changes, headache, nausea and vomiting, tiredness, muscle spasms, and seizures.

Severe hyponatremia can lead to coma and can be fatal.

Treatment of hyponatremia involves intravenous fluid and electrolyte replacement, medications to manage the symptoms of hyponatremia, as well as any treatments for the underlying cause.

bonnieh

Posted by @bonnieh, Feb 10, 2012

What are the symptoms of hyponatremia (low blood sodium)?

When sodium levels in the body are low, water tends to enter cells, causing them to swell. When this occurs in the brain, it is referred to as cerebral edema. Cerebral edema is particularly dangerous because the brain is confined in the skull without room for expansion, and the swelling can lead to brain damage as the pressure increases within the skull.

In chronic hyponatremia, in which the blood sodium levels drop gradually over time, symptoms are typically less severe than with acute hyponatremia (a sudden drop in blood sodium level). Symptoms can be very nonspecific and can include:

headache,

confusion or altered mental state,

seizures, and

decreased consciousness which can proceed to coma and death.
Other possible symptoms include:

restlessness,

muscle spasms or cramps,

weakness, and tiredness.
Nausea and vomiting may accompany any of the symptoms.

How is hyponatremia (low blood sodium)diagnosed?

The symptoms of hyponatremia are nonspecific, so a blood test measuring the sodium level is required to confirm the diagnosis of hyponatremia. Sometimes the medical history (such as prolonged vomiting or excessive sweating) will suggest the diagnosis. In other cases, further blood tests, urine tests, and imaging studies may be needed in order to determine the exact cause of the hyponatremia.

bonnieh

Posted by @bonnieh, Feb 10, 2012

Sodium: (Normal range: 136 - 145 meq/l)

Sodium plays a vital role in maintaining the concentration and volume of the extracellular fluid (ECF). It is the main cation of the ECF and a major determinant of ECF osmolality. Sodium is important in maintaining irritability and conduction of nerve and muscle tissue and assists with the regulation of acid-base balance. The average daily intake far exceeds the normal daily requirements. The kidneys are responsible for excreting the excess and are capable of conserving sodium during periods of extreme sodium restriction. The kidneys accomplish this primarily through regulation of water intake/excretion. If the serum sodium falls, the kidneys respond by excreting water. If the serum sodium increases (increased osmolality)---thirst center is stimulated--increased ADH release by the posterior pituitary---acts on kidney to conserve water. Aldosterone also plays a key role by regulating Na+/ECF volume. Its release causes the kidneys to conserve water and sodium which results in increased ECF volume. Because changes in serum sodium levels typically reflect changes in body water balance, gains or losses of total body sodium are not necessarily reflected by the serum sodium level.
Hyponatremia: (Serum sodium less than 136 meq/L)
Clinical indicators and treatment depend on the cause of hyponatremia and whether or not it is associated with a normal, decreased or increased ECF volume.
Signs and symptoms: neurologic symptoms usually do not occur until the serum sodium level has dropped to approximately 120-125 meq/L. Hyponatremia with decreased ECF volume: irritability, apprehension, dizziness, postural hypotension, dry mucus membranes, cold and clammy skin, tremors, seizures. Hyponatremia with normal or increased ECF volume: headache, lassitude, apathy, confusion, weakness, edema, weight gain, elevated blood pressure, muscle cramps, convulsions.
History and risk factors: diarrhea, fistulas, vomiting, NG suction, diuretics, adrenal insufficiency, skin losses (burns, wound drainage), other. Note: hyperlipidemia, hyperproteinemia, and hyperglycemia may cause a pseudo-hyponatremia. This must be ruled out before determining therapy. For every 100 mg/dl increase in glucose, the sodium is diluted by 1.6 meq/L.
Diagnostic tests: serum sodium will be less than 136 meq/L. Serum osmolality will be decreased except in cases of pseudo-hyponatremia, azotemia, or toxins that increase osmolality (example: ethanol). Urine specific gravity will be decreased because of the kidneys attempt to excrete excess water. Urine sodium: decreased (except in SIADH and adrenal insufficiency).
Collaborative management: The goal of therapy is to get the patient out of immediate danger (eg return the sodium level to greater than 120 meq/L) and then gradually return the serum sodium to a normal level and restore normal ECF volume.

bonnieh

Posted by @bonnieh, Feb 10, 2012

Hypervolemia: low serum serum osmolality ( 120 meq/L): Water restriction (limit to 500 to 1500 ml/ 24 hours) and furosemide 40-80 IV/ oral once daily (20-400 mg/day).
2) Patients with CHF, cirrhosis, nephrotic syndrome who usually have excessive ECF volume have few symptoms referable to hyponatremia. Usually water restriction combined with treatment of the underlying disorder is successful.
3) If severe symptomatic hyponatremia is present (sodium level < 115 meq/L) in the volume overloaded patient: Continue water restriction. Also infuse 3% hypertonic saline.
Calculate sodium deficit: 0.6 x (weight in kg) x (desired sodium - Actual sodium)
Use 0.5 for females. Desired range= 120 - 125 meq/L.
When hyponatremia is symptomatic and acute (< 24 hours in duration), the serum sodium may be raised safely to 120-125 meq/L in 24 hours or less. In patients with symptomatic chronic hyponatremia, or hyponatremia of unknown duration, the serum sodium should be raised slowly (0.5 meq/L/hr) to about 120-125 meq/L in order to avoid CNS complications (cerebral edema, pontine myelinolysis, seizures) and/or pulmonary edema. The total increase in these patients should not exceed 10-12 meq/L in 24 hours or <20-25 meq/L over 48 hours. Thereafter, the hypertonic saline is stopped, and the serum sodium is allowed to rise more slowly (eg over several days) in response to continued restriction of free water. In all cases, the serum sodium should be corrected only halfway to normal in the initial 24 hours (120-125 meq/L) to prevent the complications listed above.

Example calculations:
80kg patient; serum sodium=110 meqL ; male; desired target= 120 meq/L.
1) 0.6 x 80kg x (120-110)= 480 meq (total needed)
2) Amount needed to increase serum level by 0.5 meq/L/hr =
0.6 x 80 x 0.5= 24 meq. (rate should be 24 meq/hr)
3) 3% hypertonic saline contains 513 meq/Liter
[desired rate/hr]/513 x 1000= # ml/hr // Total meq/rate/hr
=infusion time.

Therefore: 24 meq/hr x 1000= 47 ml/hr
513
Length of infusion= 480 meq/ 24 meq= 20 hours
Final order: infuse 3% hypertonic saline at 47 ml/hr for 20 hours.
When infusion is complete, discontinue. Continue with fluid
restriction.
Hyponatremia with isovolemia
Low osmolarity ( 20: SIADH, hypothyroidism, renal failure, addisons disease, drugs.
Mild: (serum level > 120 meq/L; asymptomatic): furosemide 80mg IV once or twice daily and Normal saline + 20-40meq KCL/liter infused at 65-150 ml/hr (correct deficit at 0.5 meq/L/hr or less.)
SIADH: fluid restriction 500-750ml/ day. Demeclocycline 300 to 600mg twice daily. Use caution in patients with hepatic disease. In emergency situations (sodium < 115) use hypertonic saline (see above) and furosemide.
Symptomatic patients: hypertonic saline and furosemide as above. or hypertonic saline and water restriction.

Hyponatremia with hypovolemia
Low serum osmolarity ( 20: diuretics, renal injury, RTA, adrenal insufficiency.
If volume depleted give 500 to 3000 ml of normal saline at 500 ml/hr until no longer orthostatic, then give normal saline ( + 20-40 meq KCL/ liter) at 65 to 150 ml/hr until desired level is reached (note: in mild cases, target a level of 130 meq/ Liter). Each liter of normal saline contains 154 meq. May use the calculations above to determine approximate length of therapy. If severe hyponatremia is present (<115 meq/L) start hypertonic saline using the dosing guidelines above.

bonnieh

Posted by @bonnieh, Feb 10, 2012

The above mentioned is only a hypothetical and mathematical example of how it may work and of what is all involved.

bonnieh

Posted by @bonnieh, Feb 22, 2012

It's important to note that drinking water is a healthy habit, and our bodies absolutely require water to function. Drinking the recommended eight glasses of water per day will not lead to electrolyte imbalances or hyponatremia. Hyponatremia is only a danger when extremely high volumes of fluid are lost and replaced with water - for example, when athletes engage in vigorous activity for a protracted time (such as in marathons or triathlons), or when any strenuous physical activity is carried out in very hot temperatures.

In one study, 62 out of 488 runners in the Boston marathon who gave blood samples at the finish line had abnormally low blood sodium levels. Hyponatremia was more common in the thinnest runners - those with a body mass index (BMI) of about 20 - than in runners of normal weight. Hyponatremia tended not to affect the fastest runners (those who finished the marathon in about two hours) and was more common in those who took four hours or more to finish the race.

Hyponatremia is a medical emergency, and persons with suspected exercise-associated hyponatremia should receive immediate emergency care.

To prevent hyponatremia and electrolyte imbalances, athletes should replace lost body fluid with drinks that contain electrolytes, such as sports drinks.

bonnieh

Posted by @bonnieh, Feb 22, 2012

[Hyponatremia in ultraendurance exercises. Effects on health and performance].

Abstract
Dehydration is one of the main problems associated to endurance sports. In order to avoid the negative effects of dehydration athletes tend to drink well above their current needs. The negative effect of drinking too much fluid is hyponatremia. Hyponatremia is defined as a plasma sodium concentration lower than 135 mmol/L. Hyponatremia is the first cause of severe illness in ultraendurance sports and has been associated with sudden death. In this article, we analyze the causes, consequences, associated factors, therapeutic treatment and prevention of ultraendurance sports-associated hyponatremia. It is concluded that an adequate fluid ingestion is the best method to avoid hyponatremia. There is not conclusive data about the amount and necessity of sodium supplementation to avoid hyponatremia. However, it might be that it is not necessary to ingest additional sodium to prevent the development of hyponatremia in athletes who only partially replace their fluid losses during prolonged exercise.

bonnieh

Posted by @bonnieh, Feb 22, 2012

Who is most at risk for exercise-associated hyponatremia?

Exercise-associated hyponatremia is most common in small female endurance athletes who avidly drink water before and during endurance events such as marathons.

But large athletes are not immune to hyponatremia – and anyone who drinks enough water in a short period of time is at risk. This happened a few years back when an NFL lineman drank an estimated four gallons of water in one day during summer training camp and ended up with severe hyponatremia. He was fortunate to survive.

In addition, just as sweat rate differs, the amount of salt in sweat varies from one person to another. The term “salty sweating” refers to excess sodium in sweat. Individuals with salty sweat may be at greater risk for hyponatremia. Clues to excess salt in sweat include salty white residue on dark clothes worn during exercise and sweat that stings eyes, abrasions or cuts.

bonnieh

Posted by @bonnieh, Feb 22, 2012

Is it possible to be both dehydrated and hyponatremic at the same time?

Yes, strangely enough, it is possible, even though it seems counterintuitive. Hyponatremia is most often a disorder of drinking too much, which is why hyponatremia is sometimes referred to as water intoxication. But dehydrated athletes can also suffer from hyponatremia if they lose enough sodium in their sweat and drink enough water to dilute the blood to hyponatremic levels.

For example, if an athlete loses 10 liters of salty sweat during an Ironman-distance triathlon and drinks eight liters of plain water, the athlete will be both dehydrated and hyponatremic due to the combination of salt loss and water intake.

bonnieh

Posted by @bonnieh, Feb 22, 2012

How much and what should athletes drink during exercise?

Individual hydration needs vary quite a bit because people sweat at different rates, even during the same activity. That’s why coaches should encourage athletes to periodically weigh themselves before and after practices. Weight loss signals drinking too little, while weight gain signals drinking too much. After weighing in and out for a few practices, athletes get a quick sense of how much they should drink to minimize weight loss (dehydration) during exercise. Some athletes may need to drink only six ounces of fluid each hour, while a teammate may need 48 ounces or more to maintain hydration. When sweat losses are light and performance is not a concern, drinking plain water is fine. But on those occasions when sweat losses are high and athletes want to get the most from their bodies, sports drinks provide additional benefits.

bonnieh

Posted by @bonnieh, Feb 22, 2012

How can athletes monitor hydration status?

In addition to periodically weighing themselves before and after practices, athletes can monitor the color and volume of their urine. In a well-hydrated person, urine looks more like lemonade than apple juice. When dehydrated, the body tries hard to hold onto fluid, so urine volume is small. An athlete who excretes a small volume of dark urine is most likely dehydrated. Some sports teams have color-coded urine charts hanging above urinals and in stalls to remind athletes to pay attention to urine color.

bonnieh

Posted by @bonnieh, Feb 22, 2012

When do sports drinks offer advantages over plain water?

A well-formulated sports drink is simply water with additional benefits for athletes. Keep in mind that sports drinks are roughly 94% water, with carbohydrates and electrolytes making up most of the remaining 6%.

For athletes, there are many occasions when sports drinks provide benefits beyond water. For example, voluntary fluid intake is better with sports drinks than with water, reducing the risk of dehydration. Sports drinks do a better job of maintaining blood volume and reducing urine loss than water. And sports drinks provide a quick source of carbohydrate energy that active muscles can use to keep going longer and stronger. When athletes work up a sweat during prolonged, intense physical activity and want to get the most out of their bodies, sports drinks offer additional benefits that plain water doesn’t provide. For individuals who want to replace fluid and electrolytes but not calories during exercise, zero-calorie sports drinks are an option.

bonnieh

Posted by @bonnieh, Feb 22, 2012

In summary, how can physically active people reduce their risk for exercise-associated hyponatremia?

The best hydration advice for anyone who works up a sweat – regardless of the activity – is to drink enough during physical activity to minimize dehydration, but don’t over-drink.

The very best way to gauge fluid needs is to weigh in before and after physical activity. Weight loss signals dehydration, especially loss of more than two percent of body weight. Weight gain is a sure sign of over-drinking and a clear warning to cut back on fluid intake. Athletes who sweat for prolonged periods should also be encouraged to consume sports drinks with sodium during exercise and to avoid restricting dietary sodium.

bonnieh

Posted by @bonnieh, Feb 23, 2012


Hyponatremia is the medical term for a state of low sodium in the body, a condition common among endurance athletes. Rice University experts estimate 30 percent of the athletes in the Hawaii Ironman suffer from hyponatremia. Hyponatremia can be dangerous and even deadly if left untreated. Recognizing the early signs and symptoms of hyponatremia is the best approach to diagnosis and to the prevention of adverse sequelae.

Athletes are especially prone to developing hyponatremia. Most cases in athletes are due to either a loss of sodium from the body through perspiration or a dilution of bodily fluids from increased water intake during exercise. The amount of perspiration lost during exercise depends on several factors, including the temperature of the environment, exercise intensity, heat acclimatization and the size of the athlete. Cross-country runners have one of the highest sweat rates, 1.77 liters per hour. Other potential contributors to hyponatremia include diuretic medications, vomiting, diarrhea, congestive heart failure, syndrome of inappropriate antidiuretic hormone, liver cirrhosis, burns and kidney disease.

The best way to prevent symptoms of hyponatremia is to achieve a balance in pre-exercise hydration status. Athletes should strive to drink 5 to 7 millimeters of fluids per kilogram of body weight a minimum of four hours prior to exercise. Recommended fluid consumption during exercise varies according to several factors, including duration of the activity, temperature of the environment, exercise intensity and body weight. The most accurate way to determine your appropriate fluid intake during exercise is to measure your body weight before and after exercise. For every kilogram of weight lost, 1.5 liters of fluids should be consumed. The type of fluid consumed during exercise is important also. The American College of Sports Medicine promotes the guidelines of the Institute of Medicine, which recommends sports fluids consisting of 2 to 5 milliequivalents of potassium per liter, 20 to 30 milliequivalents of sodium per liter and 5 to 10 percent carbohydrates.

bonnieh

Posted by @bonnieh, Feb 23, 2012


Prevent Hyponatremia During Exercise Lasting Four Hours Or Longer
Dangerous drop in blood sodium levels can lead to seizures, coma, death.

Hyponatremia occurs where sodium levels in the blood become dangerously low due to excessivewater consumption. Blood sodium levels that drop too low can lead to seizures, coma, and even death. To prevent hyponatremia during endurance and ultra-endurance events lasting longer than 4 hours (such triathlons, ultra-marathons, long distance cycling, or, for slow marathon runners, a regular marathon), your child should observe the following guidelines:

•Avoid water loading before the event. There is no need for your child to try to superhydrate before the event; his body can absorb only such fluid, and if he overdrinks, he then may need to (inconveniently) urinate during the race;

•Eat salted foods and fluids (soup, pretzels, salted oatmeal) 90 minutes before exercise;

•Drink an endurance sports drink with higher sodium amounts than the standard sports drink;

•Consume salty foods during the endurance event, as tolerated (vegetable juice, broth, pickles, cheese sticks);

•Stop drinking water during exercise if the stomach is "sloshing," as may happen if the athlete drinks more than a quart (32 oz. or 1 liter) of water per hour for extended periods.

bonnieh

Posted by @bonnieh, Feb 23, 2012

Sodium - Salt - Needs for Ultra-Endurance Athletes
The right amount of sodium is sometimes helpful for athletes

High salt (sodium) diets have been linked to a number of health risks in many Americans. However, some athletes, due to their increased activity and excessive sweat production, are actually at risk of having too little sodium in their blood stream during training and competition and may have special sodium requirements. Because sodium is lost in sweat, it is more important for individuals who exercise at high intensity to get adequate sodium before, during and after exercise. This is even more critical during ultra-endurance competition.
Risks of Hyponatremia | Water Intoxication
Hyponatremia, a low concentration of sodium in the blood, has become more prevalent in ultra-endurance athletes. The Hawaii Ironman Triathlon routinely sees finishers with low blood sodium concentrations. Adequate sodium balance is necessary for transmitting nerve impulses and proper muscle function, and even a slight depletion of this concentration can cause problems. Ultra distance running events that take place in hot, humid conditions, and have athletes competing at high intensity have conditions prime for hyponatremia to develop.

Causes of Hyponatremia
During high intensity exercise, sodium is lost along with sweat. An athlete who only replaces the lost fluid with water will contribute to a decreased blood sodium concentration. As an example, consider a full glass of salt-water. If you dump out half of the contents of the glass (as is lost in sweat), and replace that with water only, the sodium concentration of in the glass is far less and the water is more dilute. This often occurs in the bloodstream of an athlete who only hydrates with water during excessive sweating. The result is hyponatremia.

Studies have shown that ultra-endurance athletes can lose 1-2 grams of salt per liter of sweat. If you consider that athletes may lose up to a liter (or more) of sweat each hour, you can see that over a long endurance event (12 hour race), it is not unimaginable that an athlete could sweat out a huge amount of sodium. Replacing this loss of sodium during the event is critical to performance and safety.

Symptoms of Hyponatremia
The early warning signs are often subtle and may be similar to dehydration; nausea, muscle cramps, disorientation, slurred speech, confusion, and inappropriate behavior. At this point, many athletes get into trouble by drinking water because they think they are dehydrated. In fact, water alone will increase the problem of hyponatremia. At the most extreme an athlete may experience seizures, coma, or death.

Treating Hyponatremia
At the first sign of nausea, muscle cramps, disorientation, an athlete should drink a sodium containing sports drink, such as Gatorade, or eat salty foods. If possible, an athlete should plan ahead and estimate his or her fluid loss and need for sodium replacement during the event, and stay on a hydration schedule during the race. If the symptoms are extreme, a medical professional should be seen.

Preventing Hyponatremia
The best way for an athlete to avoid such problems is to plan ahead. Tips and recommendations include:

•Use a sodium containing sports drinks during long distance, high intensity events.
•Eat salty foods before and during competition if possible.
•As there are no steadfast guidelines for everyone, it is important for an athlete to understand his or her individual fluid needs.
•Weigh yourself before and after training and drink enough sodium based sports drink to offset any fluid loss during exercise
•Increase salt intake several days prior to competition. The increased sodium concentration will allow additional hydration with water to remain balanced so that the dilution of blood sodium does not occur.
•Avoid use of aspirin, ibuprofen, and other non-steroidal anti-inflammatory agents as they may increase the risk of hyponatremia in athletes.
•Many triathletes take these medications without knowing of their detrimental effect on performance. Additionally, chronic use of these medications often mask the bodies own warning mechanisms that alert athletes to pain and injury. Athletes should be discouraged from excessive use of these medications.
Keep in mind that all athletes respond differently to exercise; fluid and sodium needs will vary accordingly. Foods that provide additional sodium include chicken noodle soup, a dill pickle, cheese, pretzels, and tomato juice.

As always, it is important to consult your physician for special considerations if you have a history of any health problems or are taking any medication for a health condition.

bonnieh

Posted by @bonnieh, Feb 23, 2012

Rule #1 - you can’t drink too much water.
Rule #2 - too much salt will kill you eventually.

If you live by those 2 rules - and you exercise / work regularly in hot weather, read on, it just might save your health.

The truth is, too much water and not enough salt can kill you. Most people know that dehydration can cause serious health consequences. What most don’t realize is that too much of a good thing — WATER — can also be dangerous, even deadly.

They call it WATER INTOXICATION or more technically HYPONATREMIA. It happens when the body’s balance of salt and water become quickly diluted. It affects the production of nerve impulses, and impairs mental processes. Cells take on extra water and expand. As they swell, they put stress on the body’s organs, particularly the brain, which has little room to expand within the skull. Sometimes Hyponatremia is caused by an underlying medical condition.

Hyponatremia isn’t unique to the military. Indeed, marathon runners, tri-athletes, even high-desert hikers all can succumb. “Most people aren’t aware of the risk of drinking too much water,” said Bob Murray, director of Gatorade Sports Science Institute. Sport drinks are engineered to replace both salt and fluids depleted during exercise. Drinking sports drinks can help; but it alone can’t maintain adequate sodium levels for people engaging in rigorous, endurance–level activity.

The point is you need to replenish not only the fluids you lose when you sweat, but the salt as well. Nothing that comes out of your body is pure water. So you’ve got to replace it with both the salt and water, Not Just Water.

Water Intoxication typically occurs over 4 to 6 hours or more. It attacks participants in High–Endurance events, such as marathons, long road marches and triathlons in which participants swim, bicycle and run long distances in non–stop succession.

WHY YOU NEED SODIUM

Sodium helps maintain the body’s electrical processes essential to transmitting nerve impulses and contracting muscles. When the body’s sodium content is depleted at the same time water level is increased, cells absorb more water and swell. Excessive water in the brain cells can cause seizures and in rare cases death.

TAKE RESPONSIBILITY

(1) If you are drinking and drinking and still feel horrible you need to let someone know.

(2) Besides setting drinking limits, you can maintain proper sodium level by eating chow hall food or MRE’s.

(3) Follow Hydration Instructions based on Activity Levels as well as Temperature Levels.

The Problems with Hyponatremia is that conditions may be accelerated by some existing physical condition such as;

(1) Cystic fibrosis – a condition that causes a person to lose large amount of sodium through sweating.

(2) Another problem is that initial symptoms of Hyponatremia – dizziness & headaches are the same for Dehydration and Heat Exhaustion. But the repeated vomiting common with Hyponatremia usually doesn’t occur with dehydration or heat exhaustion. So if they are not making a rapid recovery and vomiting. It’s recommending that they should be evacuated because they might have Hyponatremia.

Although civilian fatalities are rare, most race directors have seen cases that presented with seizures or comas and had to be hospitalized and some times put on the ventilator. While Hyponatremia is preventable, it also is highly treatable. Depending on the severity; the condition can be corrected by eating salted food or in more serious cases; by administering Saline Solution directly into the blood stream with IV. But only a small percentage require hospitalization.

Note: IV should only be administered by qualified medical personnel.

To Much of a Good thing

People have assumed that it’s difficult or impossible to get too much of a good thing and that if you drink too much your kidneys will get rid of the excess water. That’s not necessarily true. On average, during rest the body can rid itself of 1 to 1 ½ quarts of water in an hour through urination. If you drink more than that per hour, in excess of what you need, the body will retain water and dilute body fluids.

3 key factors

Physical conditioning, genetics, acclimatization to heat determines how much sodium you lose through sweat. The better your physical conditioning and the better your heat acclimation the more sodium you will retain.

How much salt you need to consume depends largely on how active you are. Athletes and Soldiers who carry a full pack 10 miles a day needs more than those whose primary job keeps them behind a desk.

The American Heart Association recommends daily intakes of no more than 2,400mg. of sodium per day, about 1 ¼ teaspoon. But Murray said; "people who are active for more than a few hour can sweat out many times that amount".

While rate vary; Murray said that for an hour’s workout at the gym most people can sweat ¾ of a quart to 1 ½ quart an hour and sometimes twice that rate. The average person will sweat about 1 gram of sodium for every quart of sweat. So those amounts should be replenished through food and sport drinks.

But Don’t Stop drinking water, you just need balance.

To help maintain the proper fluid and salt level; its advised that you weigh yourself before and after heavy physical exercises. For each pound lost, drink 1 pint of fluid. But if you weigh more you’ve drank too much. Says Armstrong former president of American College of Sports Medicine.

Telling the Difference

Although the symptoms are similar in both dehydration and Hyponatremia, there are some differences. With hyponatremia the person is more likely to vomit repeatedly than someone suffering from dehydration is. Seizures are more likely also.

New Medical Evacuation Guidelines

If the person vomits at least twice, and hasn’t shown marked recovery after 1 hour of re-hydration and continues to generally deteriorate they need medical help.

Equal Opportunity Health Risk

In the general population hyponatremia seem to occur more often in women, but it also occurs in men. People who tend to become hyponatremic are vigilant water drinkers who maintain low– salt diets. As a rule of thumb people who drink more than 3 quarts of fluids a day need to be certain to get enough salt. The dietary guidelines that recommend watching salt consumption are great for couch potatoes. But when people are physically active the rules change. And don’t think you can maintain a low– salt diet and make–up for it with sport drinks. Sport drinks aren’t salty enough.

Tips to Prevent Hyponatremia

(1) Switch to a saltier diet in anticipation of High Endurance activity, whether it’s running a marathon or a long road march.

(2) Eat pretzels over the last half of a long race or march.

(3) Favor sport drinks over water and drink 5 to 8 ounces every 15 to 20 minutes.

(4) Young, healthy and very physically active people need salt. THE EXCEPTIONS: those with high blood pressures or kidney disease.

(5) Replace the fluid you’re losing while you exercise. The best thing to drink if you want to work hard and recover quickly isn’t water. It’s a sport drink that can replenish Electrolytes and Nutrients lost through sweat.

Hyponatremia symptoms

(1) Nausea and vomiting

(2) Disorientation

(3) Lack of coordination

(4) Headaches

(5) Dizziness

(6) Looks an awful lot like those of Dehydration

How too much water makes you sick

(1) Exposure to heat and exercise: The body cools itself by sweating, carrying sodium and water out through the skin.

(2) Drinking water only: Replenishing fluids by drinking only water dilutes the sodium level in the fluid surrounding the body’s cells.

(3) Cell reaction: The relative imbalance of sodium outside the cells causes them to absorb excess water, swelling their size. If this happens to rapidly, it can inflame the lungs, swell the brain and possibly cause death.

bonnieh

Posted by @bonnieh, Feb 23, 2012

Sodium: A Closer Look

What exactly does sodium do in the body? Should I supplement with sodium when I exercise? I’ve heard of hyponatremia, but why is it so dangerous? This article will provide a better understanding of sodium as a critical electrolyte required for proper body function. Athletes have higher sodium needs compared to the general population because sodium loss escalates when one sweats. Sodium also is required for optimal hydration before, during, and after exercise; however, the specific amount is highly individual and must be practiced in training to determine appropriate supplementation. Through proper practice and planning, athletes can maintain balanced hydration and avoid many of the pitfalls of improper sodium supplementation, particularly the life-threatening condition of hyponatremia.

Sodium’s Role in the Body

Sodium is one of many electrolytes that are required for human life. The Food and Nutrition Board of the Institute of Medicine has detailed reports for the Dietary Recommended Intake (DRI) for sodium and other electrolytes. Sodium and chloride together create sodium chloride, commonly known as salt, and as such are often discussed together in nutritional resources. The body makes use of sodium in many ways: It plays a key role in muscle and nerve function, and it’s the electrolyte responsible for maintaining fluid levels in various parts of the body.

Sodium is required for the nervous system to effectively communicate with and coordinate various parts of the body. Electrical activity, or action potentials, are generated within a neuron, or nerve cell, and pass along and between neurons in a complex pattern throughout the body to coordinate numerous functions. Without proper levels of sodium, the electrical signals in nerve cells can not be established or transmitted, and the nervous system will fail to function properly.

Muscle function requires sodium in a similar, yet slightly different, manner. It is important to keep in mind that muscles require constant, low-level electrical stimulation from the nervous system to maintain form and proper function. For a muscle to contract and create a voluntary or involuntary movement, electrical input from a nerve is required. If sodium levels are inadequate for neuronal function, then a muscle cell will fail to function properly. Sodium is required intramuscularly, as well. When an action potential from a nerve reaches a muscle, sodium enters the muscle cell at the neuromuscular junction. This releases a flood of various other electrolytes and chemicals, which cause the muscle to contract. Without the appropriate levels of sodium, this flood would not occur, and a muscle cell would be incapable of contracting.

Although appropriate functioning of nerves and muscles requires sodium, it is not the absolute concentration of sodium that is critical — it’s the ratio of sodium inside a cell compared to sodium outside a cell that is important. The sodium level in the blood and extracellular space is constantly in flux, mainly due to the amount of sodium consumed and lost on a daily basis. There is a greater concentration of sodium outside a cell than inside a cell, and the ratio between the two is more important than the absolute level of sodium.

Of the many methods in which sodium can be gained and lost, the intake of food and the output of sweat and urine are the most important. Blood sodium concentrations are maintained under precise control by various metabolic mechanisms, such as:

• Stimulation of thirst
• Secretion of antidiuretic hormone (ADH)
• Secretion of aldosterone (another hormone)
• The handling of water and sodium by the kidneys

Sodium levels and free water levels (plain water with no sodium or other electrolytes) are treated by the body as separate entities; however, they are intrinsically linked. At any point, the body can have too much or too little free water, while at the same time having too much sodium or too little sodium. As an example of the precise control the body has over this balance, sodium intake varies from 0.2 g (10 mmol)/day of sodium in the Yanomamo Indians of Brazil to over 10.3 g (450 mmol)/day in Northern Japan. This reflects the capacity of the normal human body to excrete excess sodium, or conserve it by markedly reducing losses of sodium in the urine and sweat. However, these are the extreme ends of the spectrum; the current Daily Value (DV) for sodium intake is 2.4 g/day (2400 mg).

Sodium and Exercise

Sodium is the primary electrolyte lost in sweat. Therefore, when exercise exceeds one hour, the American College of Sports Medicine (ACSM) recommends consuming sodium along with fluids to replace both water and sodium lost in sweat. It is not adequate to simply take sodium tabs after a hard training session to replace lost sodium; an athlete must also consume adequate amounts of fluid with this sodium.

Sodium and water are required in appropriate ratios based on an athlete’s sweat rate. It is recommended that an athlete determine their sweat rate in various conditions (link to Sweat Rate Calculator) and consume sodium based on the amount of fluid they require. The American College of Sports Medicine recommends that people who are active for more than one hour consume 500–700 mg of sodium for every 32 oz (~1L) of water they consume. However, there are some who recommend 500–1,000 mg of sodium per 32 oz of water, or per one hour of intense exercise.

Experimental data has demonstrated that sweat rate and sodium loss is highly individual, ranging from 460–1840 mg/L of sweat. This can be further influenced by numerous other factors including genetics, fitness, acclimatization, and weather conditions. As such, both the sweat rate and the amount of sodium per oz (or liter) of sweat is highly individual. Athletes must experiment in training to find the right balance that works for their body and exercise conditions.

There are ways to directly measure the concentrations of electrolytes in an individual’s sweat. These include patches worn on the skin during exercise, which are then sent to a lab for analysis, and laboratory tests where an individual essentially exercises in a giant plastic bag, which is then rinsed down with pure water and the elements analyzed. These tests are very cumbersome and expensive, and the results are not terribly accurate or reliable. However, determining sweat rate is an inexpensive and convenient way to estimate sweat-related sodium loss. If an athlete knows how much weight they lose via sweat during a workout, they can then estimate the amount of sodium they need. This entails some trial and error, but it can work just as well as more expensive tests.

The major reason athletes use sodium supplements is to avoid muscle cramps. Although appropriate sodium levels are required for proper muscle function, there is no definitive cause for muscle cramps. Muscle cramps are commonly attributed to hypovolemia (low total body water) and/or hyponatremia (low sodium levels). For shorter athletic events, these seem to be less of a factor. But for events lasting more than four hours, an optimal nutrition plan, including hydration and sodium supplementation, seems to help prevent muscle cramps. However, it is highly individual, and can vary drastically from athlete to athlete.

Hyponatremia: A Closer Look

For endurance athletes, hypovolemic hyponatremia is a major health concern while training and racing. Hypovolemic hyponatremia happens when both the total body water levels (volemia) as well as total body sodium levels (natremia) are low. This condition develops as sodium and free water are lost, primarily via sweat and urine, and replaced by inappropriately hypotonic (low sodium) fluids, such as plain water or an electrolyte drink with too little sodium to cover the body’s sodium losses. When receptors in various parts of the body detect concentrations of sodium that are above or below the acceptable range, various mechanisms are turned on or off to either retain or excrete sodium and/or free water.

The kidneys play a central role in water and sodium balance, and certain medications, for example, nonsteroidal anti-inflammatory drugs (NSAIDs) like Advil, Motrin (ibuprofen), Aleve (naproxen), or aspirin, can hamper the kidneys’ ability to appropriately handle sodium and free water. As a result, these medications should be avoided before, during, or after a race. If you want to take a pain reliever on race day, use Tylenol (acetaminophen), as this medication is metabolized by the liver and does not have a major effect on the kidneys.

When a body’s concentration of sodium is low, the kidneys will reabsorb sodium destined for the urine back into the bloodstream. When this occurs, a concentration gradient is established, and water that was destined for the urine will “follow” sodium back into the bloodstream, as well. As a result, when there are low sodium concentrations in the blood, the body (specifically the kidneys) will try to correct the imbalance; however, it requires sodium from an outside source to fully correct the imbalance.

Osmosis (the flow of water across a semipermeable membrane that balances fluid concentration on both sides) is the culprit behind the major health risk of hyponatremia. When blood sodium concentrations fall rapidly below that of sodium concentrations inside the cells of the body (as they would in an endurance event), water flows down the concentration gradient from the blood into the cells, causing them to swell. This may be observed as edema (soft tissue swelling), which is common after a long race. Most tissues of the body are able to tolerate this swelling quite easily; the brain, however, does not. Brain tissue’s ability to swell is limited, because it is encased by the skull. Swelling on the brain — a condition known as cerebral edema — is a very serious condition, and can cause death.

Clinically significant hyponatremia is dangerous, but relatively uncommon; it presents with nonspecific symptoms, including:
• Decreased appetite
• Nausea and vomiting
• Difficulty concentrating
• Confusion
• Lethargy
• Agitation
• Headache
• Seizures

In the early stages, an athlete may feel he or she is simply dehydrated, and will drink plain water: This only worsens the problem. At the first sign of nausea, muscle cramps, or disorientation, an athlete should drink a sodium-rich sports drink or eat salty foods. If the symptoms are extreme, medical help should be sought immediately.

The goal, of course, is to never reach this point, and that is where nutrition planning and practice are key — particularly for endurance events lasting 4–5 hours.

When Your Doctor Advises You to Avoid Sodium

Sodium chloride (salt) is ubiquitous in the Western diet, and has gotten a bad reputation. While it is true that individuals with high blood pressure, kidney or cardiac problems, and other medical conditions need to avoid sodium, people that are healthy are able to process large amounts of sodium in their bodies with very little impact on their immediate health. Consuming large amounts of salt increases the sodium concentration both in the blood and outside the body’s cells (extracellular space). As a result, the body will compensate by increasing the amount of free water in the blood and extracellular space to reestablish an appropriate sodium concentration relative to that which is inside the body’s cells. This increases total volume of the blood, and potentially increases blood pressure and the amount of stress on the heart. In healthy individuals, this increase has minimal immediate impact; however, if this occurs often and chronically, negative long term consequences can result, including heart disease and vascular disease.

There are enormous amounts of sodium in many foods, particularly those that are prepackaged or served in a restaurant. For example, a single serving of many frozen dinners can contain almost 1,000 mg of sodium, almost half of one’s recommended daily intake. Individuals that are physically inactive and consume large amounts of sodium could be putting themselves at risk for health problems later in life. However, athletes lose more sodium than the average population, and as such, may have slightly higher daily sodium needs; they should therefore make sure they consume enough sodium, particularly after exercise. Sodium is an essential electrolyte, and should not be avoided: Individuals should simply be aware of how much sodium is in the foods they consume.

In addition to sodium supplementation during exercise, consuming adequate sodium before and after exercise is also important for optimal hydration. Consuming sodium in conjunction with fluid will cause an increase in total body water volume, which can help “top off the tank” before exercise or “refill the tank” after exercise. Beginning a workout or race fully hydrated helps improve performance and allows for greater fluid losses before performance is negatively impacted. In addition, consuming salty foods with fluid after a workout, when an athlete may be slightly hyponatremic, will aid in rehydration and recovery. Another good time to allow your sodium consumption to climb is in the days prior to a long race; this way, you are starting a race fully volume-loaded.

bonnieh

Posted by @bonnieh, Feb 23, 2012


A Bloated Stomach After Running

Bloating after running is not an uncommon occurrence, and it can happen to both novice and experienced runners alike. The bloating is often caused by an imbalance of fluids in your body, or you could simply be one of those individuals who has a tendency to retain fluids when exercising. If you experience bloating along with other symptoms, such as gas, abdominal pain, belching or blood in your stool, an underlying gastrointestinal disorder could be causing the bloating. Consult your doctor if this is the case.

Fluid Retention
Getting enough fluids when running is important to avoid dehydration, but it's possible to drink too much water and get over-hydrated. Both dehydration and over-hydration, along with not getting enough sodium in your diet, can cause an imbalance between the levels of sodium and fluids in your body -- a condition known as hyponatremia, or low blood sodium. When this happens, your body tries to restore the balance by retaining fluids, even if you are over-hydrated. Bloating is a common sign of mild hyponatremia, which can be especially noticeable in the abdomen, especially if you have over-hydrated. You may also experience bloating in the fingers and mild nausea.

Food Related Bloating
Eating too soon before exercising can easily lead to abdominal bloating. When you eat, your blood rushes to your stomach and intestines to assist in the digestive process. However, when you run, your blood gets shunted out to your extremities to provide oxygen to the muscles. This, of course, impairs the digestive process, which leads to abdominal bloating.

In some cases, the food you are consuming could be the source of your abdominal bloating. Some individuals don't digest certain types of food well, and abdominal bloating can result. If you are eating your problem foods just before running, this will exacerbate the digestive problems and subsequent bloating. Common culprits include dairy and wheat products.

Treatment
To avoid the bloating caused by fluid imbalance, Dr. Chris Koutures of the American Medical Society for Sports Medicine recommends drinking only when you are thirsty to avoid a forced regimen of hydration. Drink electrolyte-enhanced water or sports drinks to help replace the electrolytes lost when sweating. If you have a tendency to sweat out a lot of sodium -- indicated by a salty taste in the mouth when sweating or white marks on your clothes --, consider consuming more sodium in your diet. Consult your doctor first, however, because increasing sodium intake can lead to high blood pressure.

To avoid abdominal bloating caused by eating too soon before running, eat a smaller meal no less than two to four hours before running. If you forgot to or were unable to eat, consuming a small snack, such as an energy bar, 20 to 30 minutes before running should not cause a problem. Eat from different food groups to eliminate the possibility of a food intolerance. Consult a certified nutritional specialist to help you in the process.

Considerations
Many beginning runners' bodies treat the running as a trauma and retain water as a protective measure. This type of bloating should go away after several weeks of running consistently. If, however, you find that your abdominal bloating is not going away, even after adjusting your eating or drinking habits, consult a doctor. There are numerous issues that can cause abdominal bloating including digestive disorders and kidney problems.

bonnieh

Posted by @bonnieh, Mar 2, 2012

..4 Health Rules You Can Break Today
..By Oprah.com
..Posts..By Oprah.com | Vitality – Fri, Feb 17, 2012 6:21 PM
They're the imperatives for well-being that have been drilled into us forever--"Drink eight glasses of water a day!" "Eat nine servings of fruits and veggies!" "Stay away from red meat!" But it turns out that taking care of yourself isn't quite so black-and-white, says Harvard Medical School psychologist Alice Domar, PhD, coauthor of Live a Little! Breaking the Rules Won't Break Your Health. "Research is revealing that whoever wrote the old guidelines didn't have the whole picture, and that there are more paths to optimal health than we previously thought," Domar says. Happily, the new rules are more user-friendly than the old ones. Here, four tips to live by.
Old Rule: Drink eight glasses of water a day.
New Rule: Eat your water.
The recommendation to chug all that H2O was likely based on guidelines published in 1945. However, says Howard Murad, MD, author of The Water Secret, much of your daily requirement is contained in foods: Fruits, vegetables, beans, and cooked whole grains like oatmeal and quinoa (which soak up moisture in the pot) all deliver servings of water. And, as Murad points out, they offer the added bonus of nutrients: "Watermelon and cucumber are more than 90 percent water, but they also contain antioxidants. With a glass of water, all you get is water." You'll know you're hydrated when your urine is colorless or pale yellow and you're rarely thirsty.

bonnieh

Posted by @bonnieh, Mar 2, 2012

Hyponatremia
Hyponatremia is the technical term used to describe low sodium levels in the blood. Although rare, this condition can occur in healthy, active individuals. Left untreated, hyponatremia can result in severe nausea, vomiting, disorientation, and possibly even death.
Symptoms of Hyponatremia (from Mild to Severe):
•Bloating (puffiness),
•swollen hands and feet,
•nausea,
•vomiting,
•undue fatigue,
•restlessness,
•headache,
•confusion,
•disorientation,
•wheezy breathing,
•seizures,
•respiratory
•distress,
•coma, and
•death.
Sodium and Sweat Losses – A Few Facts First
Sodium is one of the most important electrolytes in the body. Its main functions are to maintain the correct amount of fluid inside and around body cells, as well as to assist in nerve signaling.
During physical activity an athlete’s internal body temperature rises tremendously. Sweating is the body’s way of preventing overheating. As sweat evaporates it cools the skin, which in turn cools the blood circulating throughout the body. Sweat contains mostly water and sodium.
The amount of sweat lost by athletes is highly variable, ranging from one-third of a litre to 2 ½ litres or more lost for every hour of activity. In addition, the amount of sodium in sweat varies dramatically from one person to another and can range from 115 mg to 5000 mg per litre of sweat. Exercise intensity and duration, plus the environmental conditions (hot, humid, windy) and individual differences, are all factors that will affect sweat and sodium losses during physical activity.
So What Causes Hyponatremia?
Hyponatremia is most likely to occur if, during sustained exercise (greater than 60 minutes duration), an athlete drinks excessive water, that is, a greater volume of water is consumed than sweat is lost. This scenario essentially dilutes the sodium remaining in the blood. It is most commonly experienced by modestly fit female runners who, by exercising at a very slow pace, lose relatively small amounts of sweat, yet they consume copious amounts of sport drink and/or water. Sport drinks should contain at least 500 mg of sodium per litre, indicating most commercial sport drinks should not be diluted. But when any athlete drinks to excess, even electrolyte-containing sport drinks may not contain enough sodium to prevent hyponatremia.
Although very rare, hyponatremia can also occur if a ‘salty sweater’ (a person who, for a variety of reasons, loses high-sodium in sweat) consumes too little sodium during their sustained physical activity, regardless of the amount of fluid they drink. Typical sport foods such as gels, bananas, fruit bars, and diluted sport drinks don’t contain enough sodium to replace the levels lost by these individuals, in particular when physical activities exceed four hours duration.
Factors that May Increase the Risk of Hyponatremia:
•excessive drinking (before, during and/or after exercise);
•high availability of drinking fluids (e.g. too many "fluid” stations);
•weight gain during exercise (caused by fluid consumption exceeding sweat and urine losses);
•low body weight;
•high body fatness;
•being female;
•slow running or performance pace;
•endurance event inexperience (i.e., novice endurance athletes);
•greater than 4 hours sustained exercise duration;
•unusually hot and/or humid environmental conditions;
•‘salty sweat’.
Preventing Hyponatremia
Individuals susceptible to becoming hyponatremic can easily prevent low sodium levels in their blood throughout endurance activities by taking a few precautions. Since exercise-related hyponatremia is primarily caused by consumption of fluids in excess of sweat and urinary losses, the most important strategy would be to avoid over consumption of fluids (especially plain water) before, during and/or after exercise.
Drink According to Thirst During Exercise
To reduce the risk of excess fluid retention during exercise, athletes should drink the amount of fluid needed only to quench their thirst. They should therefore expect to lose up to a maximum 2% of their body weight through sweat during physical activity. Some experts advise fluid intake should range between 400–800 ml for every hour of activity and discourage excessive fluid consumption at fluid stations placed too frequently throughout endurance events.
Avoid Weight Gain During Exercise
Endurance athletes should carefully monitor their weight immediately before and after their physical activity to determine their weight difference as a result of sweat loss during exercise. Weight loss greater than 2% of body weight indicates excessive dehydration; weight gain during exercise is associated with excessive fluid intake and increased risk of hyponatremia.
After exercise, athletes should drink approximately 450–675 ml of fluid for 0.5 kg of body weight lost from exercising; rehydrating until the point when urine is pale in colour intensity (i.e., pale like lemon juice).
Encourage Sodium Rich Foods
Individuals at risk of hyponatremia and those who typically lose large amounts of sweat should be encouraged to consume sodium-rich foods before, during, and after their sustained activities. Examples include sport drinks, soups, dairy products, pretzels, vegetable and tomato juices, soy sauce, pickles, other condiments, and adding salt to food during cooking or at the table.
If an athlete has suspected symptoms of hyponatremia they should seek immediate medical attention to manage this condition.

bonnieh

Posted by @bonnieh, Mar 11, 2012

So sorry for not having any more updates recently. i've been down for the past few days with a terrible cold. will be back on track soon. also, i've been gathering more info as the days go by,learned a couple more things i can update with when i get back on track. thank you for still viewing my page and giving support. have a nice day everyone.

bonnieh

Posted by @bonnieh, Mar 23, 2012

Hyponatremia is a metabolic condition in which there is not enough sodium (salt) in the body fluids outside the cells.

Causes: Sodium is found mostly in the body fluids outside the cells. It is very important for maintaining blood pressure. Sodium is also needed for nerves and muscles to work properly.

When the amount of sodium in fluids outside cells drops, water moves into the cells to balance the levels. This causes the cells to swell with too much water. Although most cells can handle this swelling, brain cells cannot, because the skull bones confine them. Brain swelling causes most of the symptoms of hyponatremia.

In hyponatremia, the imbalance of water to salt is caused by one of three conditions:

•Euvolemic hyponatremia -- total body water increases, but the body's sodium content stays the same
•Hypervolemic hyponatremia -- both sodium and water content in the body increase, but the water gain is greater
•Hypovolemic hyponatremia -- water and sodium are both lost from the body, but the sodium loss is greater
Hyponatremia is the most common electrolyte disorder in the United States

bonnieh

Posted by @bonnieh, Mar 23, 2012

“About a quarter-mile from the finish, I started to sprint. I could feel muscle twitches in my quads, and my quads were burning. I had to slow down as I felt the cramp coming on. Then wham! Like a sledgehammer to my leg, the cramp hit and I had to stop and rub it out. What could I have done to prevent that muscle cramp?”
This is a common question among athletes. Muscle cramps are involuntary, intensely painful muscle contractions that nearly every athlete has experienced at some point. Some people experience them often and simply seem to be prone to muscle cramps.
What Can You Do?
Cramps usually hit at the end of intense workouts or during endurance events because fatigued muscles are more likely to cramp. Novice athletes are more likely to have cramps as they fatigue more quickly than seasoned exercisers. If you carefully progress your workouts, you will avoid unnecessary cramps. Heat, and not being used to the heat, increases the frequency of cramps. When the season changes and summer arrives, ease into workouts in the heat.
Additionally, carefully plan your fluids, electrolytes and carbohydrate intake to help avoid or delay muscle cramps.
Are You Drinking Enough?
Studies on fluids and cramps have produced mixed results. Some studies find no associations, while other show that consuming fluids and electrolytes to avoid dehydration will prevent, or at least delay, muscle cramps. The benefits of avoiding dehydration are widespread, so even if it’s not 100 percent guaranteed that you won’t cramp, consuming adequate fluids during exercise will still improve performance.
How would dehydration cause muscle cramps? Fluids in the body are either inside the cell or outside of the cell. When we become dehydrated, the fluid outside of the cells decreases. Reductions in fluids cause nerve endings to be squished together, overexcited, and spontaneously discharge. That spontaneous discharge is a muscle twitch, which can lead to a muscle cramp. By maintaining proper hydration, you can prevent dramatic shifts in fluids that contribute to abnormal muscle contractions.
To prevent dehydration, start by drinking fluids according to your thirst. Weigh yourself before and immediately after exercise, preferably au natural. Any change in your weight is a change in fluid balance. Weight loss greater than 2 to 3 percent of your body weight increases your risk for muscle cramps. If drinking based on thirst prevents fluctuations in your weight during exercise, then you can rely on thirst to be your hydration guide. Otherwise, you need a hydration schedule to meet your fluid needs.
The Need for Salt
Fluids aren’t alone in the task of maintaining your body’s fluid balance. Electrolytes control the shift of fluids in and out of cells. The electrolyte of most concern during exercise is sodium. Found as sodium chloride in table salt. We lose more sodium in sweat than the other electrolytes. Both water and sodium are lost in sweat. Replacement of water without sodium can lead to dangerously low blood sodium levels, called hyponatremia. Hyponatremia will also occur if you are sweating a lot and simply losing a lot of sodium in sweat. This is most likely to occur during endurance exercise or with repeated sweating throughout the day. Muscle cramps may occur when the concentration of sodium in the blood decreases; cramps can progress to a serious medical emergency when hyponatremia is not treated.
To prevent hyponatremia and the muscle cramps it may cause, sodium should be consumed with fluids. This is particularly useful for cramp-prone individuals. High sodium sports drinks can delay muscle cramps in those who cramp often. Sodium may be consumed from salty foods (such as pretzels) or through sports products.
Don't Be Afraid of Carbohydrates
Carbohydrate depletion will also lead to muscle cramps. Carbohydrates are the primary fuel used during exercise. There is a finite amount of carbohydrate stored as glycogen in our muscles to provide the energy to exercise. Once that store of glycogen has been exhausted, we are at high risk for muscle cramps. The muscle requires carbohydrate (or energy) to contract; it also needs energy to relax. When there isn’t adequate fuel circulating yet we continue to exercise and contract our muscles, muscle relaxation is impaired, and the cramp occurs.
It takes about 60 to 90 minutes of exercise to deplete glycogen stores. Therefore, it is appropriate to consume carbohydrate during any activity that will last longer than 60 to 90 minutes. Even very intense exercise lasting only 45 minutes may deplete glycogen stores. Be sure to eat a carbohydrate-rich meal or snack prior to endurance or intense exercise. Plus, you will need to consume carbohydrates through food or sports products during longer duration exercise. Consuming carbohydrates appropriately is well-worth it to prevent a muscle cramp.
Follow these five steps to prevent muscle cramps:
1.Train appropriately.
2.Acclimate yourself to the environment.
3.Consume the right amount of fluids for your body to prevent dehydration.
4.Choose salty foods or sodium rich sports products before, during and after exercise.
5.Prevent carbohydrate depletion by consuming carbohydrates before your workout and during your workout if it is longer than 60-90 minutes.

bonnieh

Posted by @bonnieh, Mar 23, 2012

There is no more perplexing problem for athletes than cramps. Muscles seem to knot up at the worst possible times during important and hard-fought competitions.
The real problem is that no one knows what causes them. There are theories. The most popular ones are that muscle cramps result from dehydration or electrolyte imbalances. These arguments seem to make sense-at least on the surface. Cramps are most common in the heat of the summer when low body-fluid levels and decreases in body salts due to sweating are likely to occur.
But the research doesn't always support these explanations. For example, in the mid-1980s 82 male runners were tested before and after a marathon for certain blood parameters considered likely causes of muscle cramps. Fifteen of the runners experienced cramps after 18 miles of the race. There was no difference, either before or after the race, in terms of blood levels of sodium, potassium, bicarbonate, hemoglobin or hematocrit. There were also no differences in blood volume between the crampers and the non-crampers. Nor were there any significant differences in the way the two groups trained.
For very long events, those lasting more than about four hours, a bit more is known. A few studies have linked these cramps to hyponatremia-low sodium levels. This condition may result from drinking large volumes of fluids that are low in sodium and may be aggravated by starting the event with low levels of sodium. Since serious athletes are particularly good at avoiding the use of salt on food, they may be highly susceptible to hyponatremia. The day before and the morning of a long race it may be a good idea to use salt more liberally to increase the body's levels. The sports drink used for the race should also provide adequate levels of sodium. For long races, eating salty foods may also help prevent not only cramping, but also the life-threatening symptoms of hyponatremia.
It's interesting to note that athletes are not the only people who experience muscle cramping. Workers in occupations that require chronic use of a muscle, especially one that crosses two joints, but don't sweat profusely as athletes do, are also susceptible. A good example is musicians who are known to cramp in the hands and arms.
So if it isn't dehydration or electrolyte imbalance, what causes cramping? Other theories are emerging. One is that poor posture or inefficient biomechanics are a cause. Poor movement patterns may cause a disturbance in the activity of the Golgi tendon organs. These are "strain gauges" built into the tendon to prevent muscle tears. When activated, these organs cause the threatened muscle to relax while stimulating the antagonistic muscle-the one that moves the joint in the opposite way-to fire. There may be some quirk of body mechanics that upsets a Golgi device and sets off the cramping pattern.
If this is the cause, prevention may involve improving biomechanics, and regular stretching and strengthening of muscles that seem to cramp along with their antagonistic muscles.
Another theory is that they result from burning protein for fuel in the absence of readily available carbohydrate. In fact, one study supports such a notion. In this research, muscle cramps occurred in subjects who reached the highest levels of ammonia release during exercise. High ammonia levels indicate that protein is being used to fuel the muscles during exercise. This may indicate a need for greater carbohydrate stores before, and replacement of those stores during intense and long-lasting exercise.
When you feel a cramp coming on there are two ways to deal with it. One is to reduce the intensity and slow down-not a popular option in an important race. Another is to alternately stretch and relax the effected muscle group while continuing to move. This is difficult if not impossible to do in some sports such as running and with certain muscles. Actually there is a third option which some athletes swear by-pinching the upper lip. Who knows, it may work for you.

bonnieh

Posted by @bonnieh, Mar 23, 2012

Heat cramps are often times those annoyingly painful, short-lived episodes that can interrupt a perfectly good aerobic class. The pathophysiology behind heat cramps is poorly understood and possibly multi-factorial, but most likely related to an electrolyte imbalance. Heat cramps are brief self-limiting muscle cramps by definition, usually associated with spasm and/or involuntary jerking. They usually occur during exercise in a very hot environment and can even begin a few hours after the activity has stopped. Muscle groups typically involved include the calves, thighs and shoulders.
Heat cramps most commonly occur in deconditioned individuals, those that consume a great deal of free water or fluids devoid of salts prior to intense or vigorous exercise in a hot environment. Occasionally these cramps are seen in the experienced or seasoned athlete who has aggressively “hydrated” prior to big events such as a marathon run or long course triathlon. Less often, but not uncommon are the manifestation of these type of cramps in daylong aerobic exercise symposium classes.
Most heat cramps occur when there is an imbalance of the electrolyte sodium (Na). Sodium is a crucial element in muscle physiology, when levels drop drastically there tends to be abnormal function of the muscles and nerve tissues. Severe abnormalities in serum electrolytes can cause mental status changes and even death in the most sever cases. While severe symptoms of low sodium are rarely seen in an aerobics class, but muscle cramping is not an uncommon event. These symptoms are signs of milder electrolyte imbalance on the continuum from mild to severe imbalance.
Sodium levels in the serum (blood) are maintained under very precise control by mechanisms that involve thirst, a hormone called the antidiuretic hormone (ADH), the renin-angiotensin-aldosterone system involving the adrenal glands, and the renal (kidney) process of filtering sodium (either by excretion or retention). The medical term for low sodium osmolarity in the blood is hyponatremia. There are several ways in which hyponatremia can occur.
Low serum sodium can occur when there is a drastic loss of total body water, with a total body sodium decrease greater than that of the water loss. This is known as hypovolemic hyponatremia. This state can occur when an individual is ill, say with vomiting or diarrhea, and is not able to replace and retain fluids. Euvolemic hyponatremia is a process where the total body water increases while sodium levels remain constant, but no edema occurs. Edema is the swelling of dependent extremities, such as swollen hands, ankles and feet. We can see this process with over zealous hydration with free water (water devoid of minerals); say in someone about to run a marathon. These athletes consume too much water (without any salts) and thus change the blood sodium content. This type of hyponatremia can have catastrophic consequences before such a stressful event. For the unconditioned aerobics class participant, even less drastic over hydration can cause symptoms, due to the bodies inability to make rapid adjustment. With conditioning, compensatory mechanisms are quicker to act and more efficient.
Hypervoilemic hyponatremia occurs in people with a sodium retention problem. Take for example a person with a sick heart (Congestive Heart Failure) and lets say they increase the body sodium by too liberal an intake of table salt (something their physician probably discourages). In these individuals we see an increase in total body sodium followed by a disproportionably larger increase in the water content (due to osmosis) and edema ensues. This is where the free water is shifted out of circulation (from the vessels to the peripheral tissues), resulting in a relative rise in the serum sodium level. In medicine we call this “third spacing of fluid” and it can place a heart patient in the Intensive Care Unit. With severe peripheral edema and “fluid on the lungs” (pulmonary edema) making it difficult for oxygen exchange to occur in the lungs, these patients need supplemental oxygen and medication like diuretics to remove the excess fluid.
The process of maintaining correct levels of serum sodium and osmolarity occur through some very complex pathways. A simple breakdown of this process can be explained as follows. An increase in serum osmolarity (the concentration of salts in blood) above the normal range of 280 – 300 mOsm/kg will stimulate receptors in the hypothalamus to turn on Anti Diuretic Hormone (ADH). ADH is a hormone that reduces urine output. In times of stress where water intake is limited or there is pending dehydration, this hormone “holds onto” water. ADH increases free water reabsorption from the urine in the kidneys and as a result urine output drops. This process tries to correct the high sodium by dilution with water. A common drug that inhibits ADH is alcohol. When an individual consumes too much alcohol, the common side effect of increased urination occurs. This can rapidly dehydrate a person and this is what causes the “hang over” effect many experience the morning after binge drinking.
Aldosterone is another hormone synthesized with effects on maintaining water balance. This hormone is produced in the adrenal cortex (a small gland over the kidneys) and causes the kidneys to hold onto sodium and thus free water by osmosis helping to correct a hypovolemic state. The kidneys organ can in and of itself control sodium levels independent of both ADH and Aldosterone by increasing or decreasing tubular sodium reabsorption in times of stress (such as hemorrhage or dehydration).
The rate of development of hyponatremia plays a critical role in its pathophysiology. When serum sodium falls slowly, over a period of several days or weeks, the brain is capable of compensating up to a certain limit of course. Compensatory extrusion of solutes reduces the flow of free water into the intracellular space, and symptoms are much milder for a given degree of hyponatremia.
When serum sodium falls rapidly, over a period of 24-48 hours, this compensatory mechanism is overwhelmed and severe cerebral (brain) edema may ensue, resulting in brainstem herniation and death in extreme cases. This may only appears in very extreme cases and in the relatively very sick person. For the purpose of this article we will stress the more commonly seen phenomenon of peripheral pathophysiology, namely that noted in muscle tissues as manifest in the “cramping” phenomenon. This milder presentation is more commonly seen in an aerobics class or on the floor of a health club.
Hyponatremia is not gender specific, it can occur in women as equally as men.
People stricken with a condition called Addison’s Disease (low adrenal gland function) have a problem maintaining adequate levels of sodium, thus predisposing them to hyponatremia. The elderly have a diminished sense of thirst and may not have a fully functional hormonal compensatory mechanism, as you would see in a younger athlete. So the elderly athlete is more susceptible. Hyponatremia may be seen in association with numerous medications. Some of these medications include but are not limited to: diuretics (used in the treatment of hypertension and fluid retention), Selective Serotonin Reuptake Inhibitors (SSRI) [Some common examples of the SSRI class of drugs are Zoloft, Paxil, & Celexa], certain asthma medications and pain medications (Motrin, Non-steroidals). Also those more sensitive to hyponatremia are people with chronic illness, neoplasms (cancer), liver disease, hypothyroidism, and asthma. Additionally, low sodium levels can be seen in those individuals with excessive consumption of beer (potomania) and the recreational use of the drug Ecstasy (MDMA). Ecstasy is known to cause severe dehydration and can be quite harmful to even the casual user.
Severe symptoms of dehydration or hypernatremia should always be referred to an emergency room for definitive correction of the electrolyte imbalance. Things an aerobics instructor or personal trainer should watch for are: anorexia (poor appetite), nausea and vomiting, confusion, lethargy, headache and seizure activity.
With hypovolemic hyponatremia, a patients has decreased total body sodium stores. If symptoms are mild to moderately severe, treatment with isotonic saline given intravenously is standard care. The frequent monitoring of serum sodium levels to ensure that intravascular sodium increases no faster than 0.5 mEq/L/hour is also observed, as rapid shifts can be problematic.
In patients with hypervolemic hyponatremia, they are noted to have increased total body sodium stores. Treatment consists of sodium and water restriction and attention to the underlying cause, which is oftentimes psychiatric (psychogenic polydipsia). Psychogenic polydipsia is a mental disorder whereby the affected drinks huge volumes of water. Euvolemic hyponatremia implies normal sodium stores and a total body excess of free water. Treatment consists of free water restriction.
Hyponatremia is physiologically significant when it indicates a state of extracellular hypo-osmolarity and a tendency for free water to shift from the vascular space (blood vessels) to the intracellular space (muscle or brain cells for example). Although cellular edema is well tolerated by most tissues, it is not very well tolerated within the rigid non-expanding confines of the skull. Therefore, clinical manifestations of severe rapid hyponatremia are related primarily to cerebral edema, seizures and coma. Muscle or heat cramps can be an early warning sign to this impending often life-threatening problem.
To avoid mild to moderate hyponatremia while exercising, it is important to remember a few points.
> Condition the body gradually. Start out with moderate exercise with adequate rest between heavier bouts of exercise so the body can have ample time to acclimate to the new physical stress of exercise. The body also needs time to recover fluid loss due to perspiration and equalize electrolytes.
>Maintain adequate hydration. Over hydration with water alone can be dangerous at extremes. This is where the use of sports drinks, that are balanced with adequate electrolytes, can be helpful. When long bouts of exercise or intense exercise in very warm environments are planned, hydration with sports drinks is a better choice than just plain water. Over hydration in anticipation of profuse sweating should be done in moderation and during the activity. Drinking throughout a two-hour class is much safer than “loading” prior to the class. Instructors should discourage the intake of large amounts of water prior to a class, but allow for short “fluid replacement” breaks throughout a program.
>Exercise in a comfortable environment if at all possible. Extreme heat will cause the bodies cooling mechanism to increase perspiration to cool the skin and core temperatures, with perspiration goes the body’s salts. Keep your aerobic exercise rooms comfortable, and limit humidity if possible.
>Keep an eye out for those participants who are elderly or who have chronic diseases. Remember, their compensatory regulatory mechanisms may not function optimally. They will usually be the first to become symptomatic.
Remembering these simple rules will keep your classes safer, with participants less likely to suffer the symptoms of heat cramps (muscle cramps) due to mild hyponatremia. Heeding these recommendations will also avoid the more dangerous consequences of severe rapid lowering of sodium levels. In closing remember, a class without muscle cramps is always a good class.

bonnieh

Posted by @bonnieh, Mar 25, 2012

We've all learned that fluid replacement is critical to replace fluids lost when exercising, but drinking pure water exclusively isn't the safest choice for those who participate in very strenuous or long-duration exercise.
When significant amounts of fluid are lost through high-intensity exercise, replacement with water alone can lead to a chemical imbalance in the body and deficiencies in electrolytes, which are nutrients critical for organ functioning. The electrolytes in our body include sodium, potassium, chloride, calcium and phosphate, but sodium is the substance of most concern when replacing fluids lost through exercising.
hyponatremia is a condition in which the body's stores of sodium are too low, and this condition can result from drinking extreme amounts of water. Hyponatremia can lead to confusion, lethargy, agitation, seizures, and in extreme cases, even death. Early symptoms are nonspecific and subtle and may include disorientation, nausea, or muscle cramps. The symptoms of hyponatremia may also mimic those of dehydration, so athletes experiencing these symptoms may be given more water to drink, further worsening the condition.

bonnieh

Posted by @bonnieh, Mar 25, 2012


A muscle spasm is an involuntary muscle contraction that occurs when the brain sends signals for the muscles to contract when it is not warranted by the body. Muscle spasms can last for minutes to hours, depending on the severity and cause of the contraction. Single muscle spasms can occur as a result of overworked or strained muscles. Multiple muscle spasms usually occur as a result of underlying medical conditions.
Hyponatremia is defined as low levels of sodium in the blood. Sodium is responsible for maintaining normal blood pressure and regulating water levels in and around the cells. When sodium is low, water levels in the body increase and the cells begin to swell. Symptoms of hyponatremia include muscle spasms, muscle weakness, nausea, vomiting, headache, confusion, lethargy, fatigue, restlessness, loss of appetite and seizures, according to MayoClinic.com. Hyponatremia can be caused by excessive water intake during exercise, hormonal changes, the use of diuretics, certain medications, severe vomiting or diarrhea, kidney diseases and heart failure. Treatment for hyponatremia consists of correcting the underlying cause of the imbalance. If sodium levels are dangerously low, sodium solutions may be administered intravenously.

bonnieh

Posted by @bonnieh, Mar 25, 2012

Electrolyte Balance
Electrolytes are positively or negatively charged particles that readily dissolve in water. The predominant positively charged electrolytes in the body are sodium, potassium, calcium, and magnesium, while negatively charged electrolytes include chloride, phosphates, and bicarbonate.
Description
Salts are chemical compounds composed of atoms that carry electrical charges. Dissolved in water, the components in a salt exist as ions. Collectively, these ions are called electrolytes. Electrolytes are dissolved in different compartments of body water including: the serum portion of the blood, inside the cells (intracellular), and out-side the cells (extracellular). The concentration of these electrolytes varies considerably from one area to the other. However, there is a narrow concentration limit of these electrolytes that the body must maintain within each of these compartments. The body transfers electrolytes intracellularly and extracellularly as required to maintain electrolyte balance. Electrolyte concentrations of extracellular fluid can be measured in a blood sample.
Function
The kidney filters electrolytes in blood and maintains a balance by excreting the proper amount in the urine. An electrolyte's concentration in a solution of dissolved salts can be measured as the amount in milliequivalents (mEq) per volume of solution (i.e. per liter). Electrolytes have many functions and roles in the body. The concentration of electrolytes must be maintained within a narrow range within the blood, otherwise deleterious physiological effects may occur. Several of the most important electrolytes will be discussed individually in the following sections.
Role in human health
Sodium balance
The largest portion of the body's sodium reserves is in the extracellular fluid, which includes the blood plasma. The kidneys function to control the sodium excreted in the urine; thus the level of sodium in the body is relatively constant on a daily basis. An upset between intake of sodium (through dietary consumption) and output (in urine and sweat) creates an imbalance, affecting the total amount of sodium in the body. Variations in the total amount of sodium are related to the volume of water found in the blood.
A decrease in the overall amount of sodium does not necessarily cause the concentration of blood sodium to fall, but may decrease blood volume. Low blood volume, such as occurs with hemorrhage, signals the kidneys to conserve both water and sodium through stimulation of aldosteone. This helps to return blood volume toward normal, by increasing the amount of extracellular fluid sodium. With an excess of sodium in the body, blood volume may rise. This increase in blood volume initiates an accumulation of extracellular fluid, often in the feet, ankles, and lower legs, resulting in a condition known as edema.
The body maintains extracellular fluid sodium concentration homeostasis through the thirst mechanism and regulation of kidney water excretion by antidiuretic hormone (ADH). When sodium concentrations opposed to too much total sodiums too high, thirst prompts water intake and, at the same time, the ADH signals to the kidneys to conserve water, by increasing water absorption by the organs and passing less water into the excretory system.
Common disorders
The electrolytes involved in disorders of salt balance are most often sodium, potassium, calcium, phosphate, and magnesium. The concentration of blood chloride is usually similar to the blood sodium concentration, while bicarbonate is related to acid-base balance.
Sodium balance
HYPONATREMIA. The most common electrolyte disorder is hyponatremia, it occurs in almost 1% of all patients hospital admissions. Hyponatremia is a condition characterized by low sodium in the blood, below 136 mEq per liter of blood. In hyponatremia, the sodium concentration has been overdiluted by an excess of water or a loss of sodium in the body. Hyponatremia may result from intraveous administration of water to hospitalized patients or can also occur with small amounts of water consumption in those who have impaired kidney function and several other conditions such as liver cirrhosis, heart failure, underactive adrenal glands as with Addison's disease, and various antidiuretic hormone disorders. Over 50% of hospitalized patients with AIDS have been reported to suffer from hyponatremia. Lethargy and confusion are typically the first signs of hyponatremia. Muscle twitching and seizures may occur as hyponatremia progresses with risk of stupor, coma, and death in the most severe cases. Due to the effects on the central nervous system, mortality risk is considerably greater in acute hyponatremia than in chronic hyponatremia. Other factors that reduce survival are the presence of debilitating illnesses such as alcoholism, hepatic cirrhosis, heart failure, or malignancy.
HYPERNATREMIA. Hypernatremia is a condition characterized by a high concentration of sodium in the blood, above 145 mEq per liter of blood. There is too little water compared to the amount of sodium in the blood, often resulting from a low intake of water. Profuse sweating, vomiting, fever, diarrhea, or abnormal kidney function may result in hypernatremia. With age, there is a decreased thirst sensation; therefore, hypernatremia is more common in the elderly. Aging reduces the kidney's ability to concentrate urine; therefore, taking diuretics may further exacerbate hypernatremia. Hypernatremia is very serious, particularly in the elderly. Almost half of individuals hospitalized for this condition will die, although it is often secondary to other illnesses.
Major causes of high sodium levels include:
•limited water access, particularly when combined with any other cause
•excess water loss due to profuse sweating, vomiting, fever, diarrhea
•disorders of other electrolytes
•head trauma or neurosurgery involving the pituitary gland
•use of drugs including lithium, diuretics, demeclocycline
•diabetes insipidus
•sickle cell disease
As with hyponatremia, the major symptoms of hypernatremia result from brain dysfunction. Severe hypernatremia can lead to confusion, muscle twitching, seizures, coma, and death. The effects on central nervous system hyperosmolality and the seriousness of the under-lying illness lead to greater mortality in acute hypernatremia compared to chronic hypernatremia.

bonnieh

Posted by @bonnieh, Apr 24, 2012

An Endocrinologist is a medical doctor who specializes in diseases of the glands. They have received additional education and clinical training in order to treat many different diseases involving hormone-secreting/excreting glands, including diabetes.

Though your primary care physician has knowledge regarding the diabetes treatment and management, an Endocrinologist - like a specialist in any other area - has the most current information, treatment guidelines and educational programs, that can help you successful take control of your disease.

So, what do Endocrinologists treat? They treat conditions of the endocrine system. The endocrine system is a complex group of glands. Glands are organs that make hormones. These are substances that help to control activities in your body. Hormones control reproduction, metabolism (food burning and waste elimination), and growth and development.

Hormones also control the way you respond to your surroundings, and they help to provide the proper amount of energy and nutrition your body needs to function. The endocrine glands include the thyroid, parathyroid, pancreas, ovaries, testes, adrenal, pituitary and hypothalamus.

Talk to your primary care physician about a referral to an Endocrinologist, to help you better care for yourself and your disease.

bonnieh

Posted by @bonnieh, Apr 24, 2012

Establishing the type of hyponatremia
The first step is to measure serum osmolality. If it is normal, the patient has pseudohyponatremia (isotonic hyponatremia), which is an artifact produced by high serum lipid or protein levels. The most common cause of high protein levels is multiple myeloma; this diagnosis is already known in the majority of patients.

If the serum osmolality is >295 mOsm/kg H2O, the patient has redistributive hyponatremia (hypertonic), which is either due to hyperglycemia or to the absorption or administration of a hypertonic fluid (e.g., mannitol, glycine, or sorbitol).

Hyperglycemia is usually caused by diabetes but can also be caused by medications (beta-blockers, thiazide diuretics, corticosteroids, niacin, pentamidine, protease inhibitors, some antipsychotics) or by stress from a recent stroke, myocardial infarction, trauma, infection, or inflammation. A fasting or random serum glucose measurement establishes hyperglycemia as the cause. The serum HbA1c is elevated in people with poorly controlled diabetes and may also be useful. Medication-induced hyponatremia and hyperglycemia should resolve once the causative agent is discontinued.

Hypertonic hyponatremia due to mannitol, glycine, or sorbitol is usually easily established by examination of fluids administered intravenously or used to irrigate the operative field during transurethral resection of prostate or hysteroscopy. However, it can be confirmed by calculation of the serum osmolar gap. http://www-users.med.cornell.edu/~spon/picu/calc/osmolal.htm [Serum osmolality calculator] A difference >10 indicates the presence of nonsodium effective osmoles such as mannitol, glycine, or sorbitol.

If the serum osmolality is <280 mOsm/kg H2O, the patient has hypotonic hyponataremia (hypovolemic, euvolemic, or hypervolemic).

Patients with hypovolemic hyponatremia will have signs of volume depletion (decreased skin turgor, reduced jugular venous pressure, decreased blood pressure).

Patients with hypervolemic hyponatremia will have an elevated jugular venous pressure and peripheral edema.

The absence of any of these signs indicates that the patient is euvolemic.

Because hyponatremia can arise in hypervolemic, euvolemic, and hypovolemic states, hyponatremia and its cause may not initially be clear. The most important test to identify the etiology in patients with hypovolemic hypotonic hyponatremia, euvolemic hypotonic hyponatremia, or hypervolemic hypotonic hyponatremia is measurement of urinary sodium. A spot urinary sodium test is available that allows urinary sodium to be quickly and conveniently measured in a random urine sample.

Hypovolemic hyponatremia: urinary sodium >20 mEq/L indicates renal sodium losses and urinary sodium ≤20 mEq/L indicates extrarenal sodium losses.

Hypervolemic hyponatremia: urinary sodium >20 mEq/L suggests chronic renal failure and a urinary sodium ≤20 mEq/L suggests edematous disorders such as heart failure, cirrhosis, or nephrotic syndrome.

Patients with euvolemic hyponatremia always have a urinary sodium >20 mEq/L.

bonnieh

Posted by @bonnieh, Apr 24, 2012

Hypovolemic hyponatremia with urinary sodium >20 mEq/L
Thiazide diuretics

The hyponatremia may appear within days or even years of starting the medication, and will resolve once thiazide diuretics have been discontinued.

Renal disease

Salt-wasting nephropathy should be considered as a cause in all patients with hypovolemic hyponatremia with a urinary sodium >20 mEq/L. Many patients will have a known diagnosis or a positive family history of tubulointerstitial disease (interstitial nephritis, medullary cystic kidney disease, partial urinary tract obstruction, and polycystic kidney disease). Salt-wasting nephropathy often precedes the onset of renal failure in these conditions. An abdominal mass is often present in polycystic kidney disease. Patients with medullary cystic kidney disease have early signs of severe anemia such as pallor.

The serum creatinine may be normal or elevated with a normal or reduced GFR. Urinalysis reveals hematuria and/or proteinuria, depending on the underlying cause. Renal ultrasound will detect obstruction, hydronephrosis, kidney stones, or cysts. Contrast-enhanced abdominal CT scanning is a more definitive imaging tool for assessing the number, size, and location of the cysts in polycystic kidney disease and medullary cystic kidney disease. Genetic testing is the definitive method for distinguishing these conditions. Renal biopsy is required for the definitive diagnosis of the interstitial nephritis, and should be considered in consultation with a renal specialist.

CNS cause

If there is a history of recent head injury, intracranial surgery, subarachnoid hemorrhage, stroke, or brain tumors, cerebral salt-wasting syndrome should be considered as the cause. These conditions can also cause SIADH, but SIADH causes euvolemic hyponatremia and is a diagnosis of exclusion. A complete history and CNS examination should identify the cause.

A CT scan brain will identify signs of hemorrhage or skull fractures. An MRI brain is the preferred modality to detect intracranial tumors and to assess ischemic stroke once hemorrhagic stroke has been excluded by CT.

Mineralocorticoid deficiency

Should also be excluded as a cause. Symptoms and signs are usually nonspecific and include nausea, vomiting, myalgia, arthralgia, and clinical signs of volume depletion.

Serum potassium is usually elevated. A decreased morning serum cortisol is diagnostic. A decreased cortisol response to ACTH is seen.

bonnieh

Posted by @bonnieh, Apr 24, 2012

Hypovolemic hyponatremia with urinary sodium ≤20 mEq/L
This is produced by inappropriate replacement of extrarenal sodium and fluid losses with hypotonic fluids. This may be caused by replacement of excessive sweating (often due to prolonged exercise in a hot environment) by oral tap water or by intravenous hypotonic fluids. These causes are evident from the history and examination of fluid charts.

Other causes of fluid loss that may prompt inappropriate fluid replacement include vomiting, diarrhea, GI fistulas or drainage tubes, and third spacing of fluids caused by peritonitis, pancreatitis, burns, or small bowel obstruction.

Hypervolemic hyponatremia with urinary sodium ≤20 mEq/L
Congestive heart failure

A history of myocardial infarction should prompt consideration of congestive heart failure. Symptoms include fatigue, decreased exercise tolerance, dyspnea on exertion, orthopnea, and paroxysmal nocturnal dyspnea. Clinical signs include edema, displaced cardiac apex, hepatojugular reflux, jugular venous distension, S3 gallop, pulmonary rales, and hepatomegaly.

Chest x-ray may show cardiomegaly, pulmonary edema, or a pleural effusion. An ECG may show anterior Q waves (indicating a previous myocardial infarction), bundle branch block, atrial arrhythmias, ventricular arrhythmias, left axis deviation, or left ventricular hypertrophy. An echocardiogram detects systolic and diastolic dysfunction. Valve lesions, signs of pericardial injury, or cardiomyopathy may also be seen.

Liver cirrhosis

A history of alcohol misuse, intravenous drug use, unprotected intercourse, obesity, blood transfusion, or known hepatitis infection should prompt suspicion of cirrhosis. Cirrhosis severe enough to cause hypervolemic hyponatremia is usually symptomatic. Symptoms include fatigue, weakness, weight gain, and pruritus. Signs include edema, jaundice, ascites, collateral circulation, hepatosplenomegaly, leukonychia, palmar erythema, spider angiomata, telengiectasia, jaundiced sclera, hepatic fetor, and altered mental status.

LFTs are abnormal, and the pattern depends on the cause of cirrhosis.

An abdominal ultrasound can be used to detect signs of advanced cirrhosis such as liver surface nodularity, small liver, possible hypertrophy of left/caudate lobe, ascites, splenomegaly, and increased diameter of the portal vein (≥13 mm) or collateral vessels. Liver biopsy provides a definitive diagnosis, but is only necessary if the diagnosis cannot be established based on clinical features, investigations, and imaging.

Nephrotic syndrome

Should be suspected if there is a history of long-standing diabetes, malignancy, SLE, HIV infection, multiple myeloma, connective tissue diseases, or amyloidosis, or use of known causative medications (pamidronate, lithium, gold, penicillamine, or nonsteroidal anti-inflammatory drugs, and, very rarely, interferon-alpha, lithium, heroin, mercury, or formaldehyde). Patients present with leg or generalized edema and foamy urine. Patients may also have Muehrcke lines (due to hypoalbuminemia) or xanthelasmas (due to hypertriglyceridemia).

Serum albumin levels are low. The plasma creatinine may be normal or elevated depending on the stage of disease. A 24-hour urine collection for protein shows nephrotic range proteinuria (>3 g/24 hours). Renal biopsy is required for the definitive diagnosis of many of the underlying causes, and should be considered in consultation with a renal specialist.

bonnieh

Posted by @bonnieh, Apr 24, 2012

Hypervolemic hyponatremia with urinary sodium >20 mEq/L
Indicates chronic renal failure with impaired sodium excretion. In most patients the diagnosis is already known, but further assessment is required if a new diagnosis of renal failure is made. Signs and symptoms of renal failure may be present and include jaundice, skin bruising, poor concentration/memory, or myoclonus.

Serum creatinine is elevated with a reduced GFR, and urinalysis reveals hematuria and/or proteinuria depending on the underlying cause. Renal ultrasound can be useful to assess the cause, and may reveal small kidneys, obstruction or hydronephrosis, and kidney stones. A kidney biopsy is required for the definitive diagnosis of intrinsic causes of renal failure, and should be considered in consultation with a renal specialist.

Euvolemic hyponatremia
Excessive oral fluid intake

If a history of schizophrenia or psychotic depression is present, psychogenic polydipsia should be considered. A history of polydipsia and polyuria is present. Patients usually complain of a persistent sensation of dry mouth. This may sometimes be due to phenothiazine medications and sometimes be due to the underlying condition. The clinical examination is usually normal, although weight gain due to high water intake may occur in extreme cases. The water intake is so excessive that it overcomes the capacity of the kidney to resorb water, and urine osmolality is <100 mOsm/kg H2O.

If a history of chronic alcohol abuse is present, beer drinker's potomania should be considered. The CAGE questionnaire can be helpful in identifying patients with alcohol abuse. A CAGE score >2 is suspicious. Beer drinker's potomania is precipitated by drinking more than 6 liters of beer a day on a background of chronic poor dietary intake. Urine osmolality is 200 units/L.

Postoperative period

A transient increase in ADH secretion occurs during this period. The hyponatremia is self-limiting. However, administration of hypotonic fluids during this time can produce a more severe or prolonged hyponatremia.

Large volumes of hypertonic fluids (glycine, mannitol, or sorbitol) are used to irrigate the operative field during transurethral resection of the prostate or hysteroscopy. If the fluid is absorbed without the solute, this can produce euvolemic hypotonic hyponatremia.

Large volumes of hypotonic fluids are used to irrigate the operative field during endometrial ablation. If absorbed, this can produce severe acute hyponatremia.

SIADH

If all other causes of euvolemic hyponatremia have been excluded, the patient has SIADH. [18]

Known drug causes include vasopressin, nonsteroidal anti-inflammatory drugs, nicotine, chlorpropamide, carbamazepine, tricyclic antidepressants, SSRIs, vincristine, thioridazine, cyclophosphamide, clofibrate, and ecstasy use.

Recent head injury, intracranial surgery, subarachnoid hemorrhage, stroke, brain tumors, meningitis, or brain abscess can cause SIADH.

A history of cough, shortness of breath, or pleuritic chest pain should prompt consideration of respiratory causes of SIADH. These include pneumonia, lung abscess, COPD, cystic fibrosis, and positive pressure ventilation.

Ectopic ADH secretion by tumors is an important cause to exclude. The most common source is small cell lung cancer; other cancers are rare causes. These include cervical cancer, lymphoma, leukemia, and pancreatic adenoma.

Appropriate investigations depend on the cause identified by the clinical features. If there is no identifiable cause, the patient is diagnosed to have idiopathic SIADH.

bonnieh

Posted by @bonnieh, May 3, 2012

sorry for no recent updates everyone. im in process of wedding planning and a few other events at the time. i will be doing more updates here within the next couple days. found some good things to start updating on, its just keeping up with all my plans and taking the time when im not so tired to update. be looking for some more updates soon.

bonnieh

Posted by @bonnieh, May 3, 2012

with encouragement from my better half, he convinced me to do updates tonight. here they are:

bonnieh

Posted by @bonnieh, May 3, 2012

Side Effects of Tegretol - for the Consumer
Tegretol
All medicines may cause side effects, but many people have no, or minor, side effects. Check with your doctor if any of these most COMMON side effects persist or become bothersome when using Tegretol:

Dizziness; drowsiness; dry mouth; nausea; unsteadiness; vomiting.

Seek medical attention right away if any of these SEVERE side effects occur when using Tegretol:
Severe allergic reactions (rash; hives; itching; difficulty breathing; tightness in the chest; swelling of the mouth, face, lips, or tongue); black, tarry, or bloody stools; calf pain, swelling, or tenderness; change in the amount of urine produced; chest pain; confusion; dark urine; decreased coordination; fainting; fast, slow, or irregular heartbeat; fever, chills, or sore throat; hallucinations; joint pain; light-headedness; loss of appetite; menstrual changes; new or worsening mental or mood changes (eg, aggression, agitation, anger, anxiety, depression, irritability, restlessness); pain, tenderness, or unusual swelling in the neck, groin, or under the arms; red or purple spots on your body; red, swollen, blistered, or peeling skin; severe or persistent dizziness or headache; severe or persistent nausea or vomiting; shortness of breath; speech problems; stomach pain; sudden, unusual weight gain; suicidal thoughts or actions; swelling of the hands, ankles, or feet; swollen lymph nodes; trouble sleeping; ulcers or sores in the mouth; uncontrolled muscle movements; unusual bruising or bleeding (eg, bleeding gums, nosebleeds); unusual tiredness or weakness; vision or eye problems; yellowing of the skin or eyes.

This is not a complete list of all side effects that may occur. If you have questions about side effects, contact your health care provider. Call your doctor for medical advice about side effects.

bonnieh

Posted by @bonnieh, May 3, 2012

Important facts about this drug:

You may develop a rash during the first 2 to 8 weeks of Carbamazepine therapy. If this happens, notify your doctor immediately. The rash could become severe and even dangerous, particularly in children. A slight possibility of this problem remains for up to 6 months.

More common side effects may include:
Blurred vision, dizziness, double vision, headache, nausea, rash, sleepiness, uncoordinated movements, vomiting

Less common side effects may include:
Abdominal pain, accidental injury, anxiety, constipation, depression, diarrhea, fever, "flu-like" symptoms, increased cough, inflammation of vagina, irritability, painful menstruation, sore throat, tremor

Rare side effects may include:
Absence of menstrual periods, chills, confusion, dry mouth, ear pain, emotional changes, heart palpitations, hot flashes, joint disorders, memory decrease, mind racing, muscle weakness, muscle spasm, poor concentration, ringing in ears, sleep disorder, speech disorder

Symptoms of Carbamazapine overdose may include:
Lack of coordination, rolling eyeballs, increased seizures, decreased level of consciousness, coma, delayed heartbeat.

bonnieh

Posted by @bonnieh, May 3, 2012

Look me up on facebook also you will also find the same things that i post on here also on my new facebook page it is titled: Hyponatremia~(Sodium Defficiency). it could really use the support.

bonnieh

Posted by @bonnieh, May 3, 2012

Carbamazepine
((The following information is an educational aid only. It is not intended as a medical advice for individual conditions or treatments. Talk to your doctor, nurse or pharmacist before following any medical regimen to see if it is safe and effective for you.))
What key warnings should I know about before taking this medicine?
Serious blood cell count problems may occur. Report any fever, sore throat, mouth sores, infections, easy bruising, or purple “splotches” on your skin to healthcare provider right away.
Serious rashes have been reported. People of Asian descent are most likely to get these. Talk with healthcare provider right away if you develop a rash.
Reasons not to take this medicine
• If you have an allergy to carbamazepine or any other part of this medicine.
• Tell healthcare provider if you are allergic to any medicine. Make sure to tell about the allergy and how it affected you. This includes telling about rash; hives; itching; shortness of breath; wheezing; cough; swelling of face, lips, tongue, or throat; or any other symptoms involved.
• If you have bone marrow disease.
• If you are taking nefazodone.
• If you have taken isocarboxazid, phenelzine, or tranylcypromine in the last 14 days. Monoamine oxidase inhibitors (eg, isocarboxazid, phenelzine, and tranylcypromine) must be stopped 14 days before this medicine is started. Taking the two together could cause dangerously high blood pressure.
• If you are pregnant or may be pregnant.
• If you are breast-feeding.
What is this medicine used for?
• This medicine is used to prevent or treat seizures.
• This medicine is used to relieve painful nerve diseases and diabetic nerve disorders.
• This medicine is used to treat drug withdrawal.
• This medicine is used to treat manic depression.
• This medicine is used to treat restless leg syndrome.
How does it work?
• Carbamazepine calms the brain.
• It is a mood stabilizer.
How is it best taken?
• Take this medicine with or without food. Take with food if it causes an upset stomach.
• Long-acting products: Swallow whole. Do not chew, break, or crush.
• Chewable tablet: Chew or crush well. Mix crushed tablet with food. Do not swallow whole.
• A liquid (suspension) is available if you cannot swallow pills. Shake well before use. Mix with an equal amount of water before drinking.
• Those who have feeding tubes can also use the liquid. Flush the feeding tube before and after medicine is given.
What do I do if I miss a dose? (does not apply to patients in the hospital)
• Take a missed dose as soon as possible.
• If it is almost time for the next dose, skip the missed dose and return to your regular schedule.
• Do not take a double dose or extra doses.
• Do not change dose or stop medicine. Talk with healthcare provider.
What are the precautions when taking this medicine?
• Wear disease medical alert identification.
• If you are 65 or older, use this medicine with caution. You could have more side effects.
• Follow laws about driving with a seizure condition.
• If you have been taking this medicine for several weeks, talk with healthcare provider before stopping. You may want to gradually withdraw this medicine.
• If you have kidney disease, talk with healthcare provider.
• If you have liver disease, talk with healthcare provider.
• Check medicines with healthcare provider. This medicine may not mix well with other medicines.
• Diltiazem, danazol, verapamil, and propoxyphene may increase this medicine's side effects. Talk with healthcare provider.
• You may not be alert. Avoid driving, doing other tasks or activities until you see how this medicine affects you.
• Do not take other liquid medicines within 2 hours of this liquid medicine.
• Avoid grapefruit and grapefruit juice.
• Avoid alcohol (includes wine, beer, and liquor).
• You can get sunburned more easily. Avoid sun, sunlamps, and tanning beds. Use sunscreen; wear protective clothing and eyewear.
• Birth control pills and other hormone-based birth control may not work to prevent pregnancy. Use another form of birth control while taking this medicine.
What are some possible side effects of this medicine?
• Feeling lightheaded, sleepy, having blurred vision, or a change in thinking clearly. Avoid driving, doing other tasks or activities that require you to be alert or have clear vision until you see how this medicine affects you.
• Change in balance.
• Nausea or vomiting. Small frequent meals, frequent mouth care, sucking hard, sugar-free candy, or chewing sugar-free gum may help.
• Dry mouth. Frequent mouth care, sucking hard, sugar-free candy, or chewing sugar-free gum may help.
What should I monitor?
• Change in condition being treated. Is it better, worse, or about the same?
• Check blood work regularly. Talk with healthcare provider.
• Dry mouth may cause an increase in cavities. Take good care of your teeth. See a dentist regularly.
• Follow up with healthcare provider.
Reasons to call healthcare provider immediately
• If you suspect an overdose, call your local poison control center or emergency department immediately.
• Signs of a life-threatening reaction. These include wheezing; chest tightness; fever; itching; bad cough; blue skin color; fits; or swelling of face, lips, tongue, or throat.
• Signs or symptoms of infection. These include a fever of 100.5 degrees or higher, chills, severe sore throat, ear or sinus pain, cough, increased sputum or change in color, painful urination, mouth sores, wound that will not heal, or anal itching or pain.
• Signs or symptoms of depression, suicidal thoughts, nervousness, emotional ups and downs, abnormal thinking, anxiety, or lack of interest in life.
• Significant change in thinking clearly and logically.
• Significant change in balance.
• Severe nausea or vomiting.
• Unusual bruising or bleeding.
• Yellow skin or eyes.
• Not hungry.
• Feeling extremely tired or weak.
• If seizures are worse or different after starting medicine.
• Any rash.
• No improvement in condition or feeling worse.
How should I store this medicine?
• Store at room temperature.
• Protect from light.
• Protect capsules and tablets from moisture. Do not store in a bathroom or kitchen.
General statements
• If you have a life-threatening allergy, wear allergy identification at all times.
• Do not share your medicine with others and do not take anyone else's medicine.
• Keep all medicine out of the reach of children and pets.
• Keep a list of all your medicines (prescription, natural products, supplements, vitamins, over-the-counter) with you. Give this list to healthcare provider (doctor, nurse, nurse practitioner, pharmacist, physician assistant).
• Call your doctor for medical advice about side effects.
• Talk with healthcare provider before starting any new medicine, including over-the-counter, natural products, or vitamins.

bonnieh

Posted by @bonnieh, May 3, 2012


Nutritional needs vary somewhat according to gender. Teenage girls and women of childbearing age need more iron in their diets than teenage boys and adult men. Sodium needs do not vary by gender, however. In fact, both males and females should limit their daily sodium intake.

Increased Iron Needs in Females
Teenage girls and women of childbearing age lose iron during menstruation. Heavy or long menstrual bleeding can deplete women's iron stores significantly, putting them at greater risk for iron deficiency anemia. Pregnant women also need more iron in their diets. Iron deficiency anemia, or a lack of healthy red blood cells, can cause weakness, fatigue, shortness of breath, decreased immune function and decreased school and work performance.

Recommended Intake
For most of childhood, girls and boys need about the same amount of iron. Children ages 1 to 3 need 7 mg of iron per day, children 4 to 8 need 10 mg per day and children 9 to 13 need 8 mg per day. Girls ages 14 to 18 need 15 mg of iron per day, while boys the same ages need only 11 mg. Women ages 19 to 50 need 18 mg of iron per day, while women 51 and over and men 19 and over need only 8 mg per day. Pregnant women need 27 mg of iron per day.

Iron Food Sources
Animal-based products such as liver, poultry, beef, oysters, tuna and salmon provide good sources of heme iron, a type of iron absorbed efficiently by the body. Plant-based iron sources, including spinach, dried beans, dried peas, whole grains and iron-fortified cereals, provide nonheme iron. Vitamin C and animal proteins aid in the body's absorption of nonheme iron.

Sodium Intake
Excess sodium in the diet can cause high blood pressure, a risk factor for heart disease. Research has linked lower sodium intake with reduced risk of hypertension, heart disease, stroke and some cancers. Both men and women should limit their daily intake of sodium to 2,300 mg, or about 1 tsp. People with high blood pressure and those with a high risk of developing high blood pressure, including adults 40 and over, African-Americans and diabetics, should limit their sodium intake to 1,500 mg per day, or about two-thirds of a teaspoon of salt. Experts at many health organizations, including the Harvard School of Public Health, the American Heart Association and the Center for Science in the Public Interest, suggest that everyone limit their daily sodium intake to 1,500 mg per day.

bonnieh

Posted by @bonnieh, May 3, 2012

Salt, energy, metabolic rate, and longevity


In the 1950s, when the pharmaceutical industry was beginning to promote some new chemicals as diuretics to replace the traditional mercury compounds, Walter Kempner’s low-salt “rice diet” began to be discussed in the medical journals and other media. The diuretics were offered for treating high blood pressure, pulmonary edema, heart failure, “idiopathic edema,” orthostatic edema and obesity, and other forms of water retention, including pregnancy, and since they functioned by causing sodium to be excreted in the urine, their sale was accompanied by advising the patients to reduce their salt intake to make the diuretic more effective.

It was clear to some physicians (and to most veterinarians) that salt restriction, especially combined with salt-losing diuresis, was very harmful during pregnancy, but that combination became standard medical practice for many years, damaging millions of babies.

Despite numerous publications showing that diuretics could cause the edematous problems that they were supposed to remedy, they have been one of the most profitable types of drug. Dietary salt restriction has become a cultural cliché, largely as a consequence of the belief that sodium causes edema and hypertension.

Salt restriction, according to a review of about 100 studies (Alderman, 2004), lowers the blood pressure a few points. But that generally doesn’t relate to better health. In one study (3000 people, 4 years), there was a clear increase in mortality in the individuals who ate less salt. An extra few grams of salt per day was associated with a 36% reduction in “coronary events” (Alderman, et al., 1995). Another study (more than 11,000 people, 22 years) also showed an inverse relation between salt intake and mortality (Alderman, et al., 1997).

Tom Brewer, an obstetrician who devoted his career to educating the public about the importance of prenatal nutrition, emphasizing adequate protein (especially milk), calories, and salt, was largely responsible for the gradual abandonment of the low-salt plus diuretics treatment for pregnant women. He explained that sodium, in association with serum albumin, is essential for maintaining blood volume. Without adequate sodium, the serum albumin is unable to keep water from leaving the blood and entering the tissues. The tissues swell as the volume of blood is reduced.

During pregnancy, the reduced blood volume doesn’t adequately nourish and oxygenate the growing fetus, and the reduced circulation to the kidneys causes them to release a signal substance (renin) that causes the blood to circulate faster, under greater pressure. A low salt diet is just one of the things that can reduce kidney circulation and stimulate renin production. Bacterial endotoxin, and other things that cause excessive capillary permeability, edema, or shock-like symptoms, will activate renin secretion.

The blood volume problem isn’t limited to the hypertension of pregnancy toxemia: “Plasma volume is usually lower in patients with essential hypertension than in normal subjects” (Tarazi, 1976).

Several studies of preeclampsia or toxemia of pregnancy showed that supplementing the diet with salt would lower the women’s blood pressure, and prevent the other complications associated with toxemia (Shanklin and Hodin, 1979).

It has been known for many years that decreasing sodium intake causes the body to respond adaptively, increasing the renin-angiotensin-aldosterone system (RAAS). The activation of this system is recognized as a factor in hypertension, kidney disease, heart failure, fibrosis of the heart, and other problems. Sodium restriction also increases serotonin, activity of the sympathetic nervous system, and plasminogen activator inhibitor type-1 (PAI-1), which contributes to the accumulation of clots and is associated with breast and prostate cancer. The sympathetic nervous system becomes hyperactive in preeclampsia (Metsaars, et al., 2006).

Despite the general knowledge of the relation of dietary salt to the RAA system, and its application by Brewer and others to the prevention of pregnancy toxemia, it isn’t common to see the information applied to other problems, such as aging and the stress-related degenerative diseases.

Many young women periodically crave salt and sugar, especially around ovulation and premenstrually, when estrogen is high. Physiologically, this is similar to the food cravings of pregnancy. Premenstrual water retention is a common problem, and physicians commonly offer the same advice to cycling women that was offered as a standard treatment for pregnant women--the avoidance of salt, sometimes with a diuretic. But when women premenstrually increase their salt intake according to their craving, the water retention can be prevented.

Blood volume changes during the normal menstrual cycle, and when the blood volume is low, it is usually because the water has moved into the tissues, causing edema. When estrogen is high, the osmolarity of the blood is low. (Courtar, et al., 2007; Stachenfeld, et al., 1999). Hypothyroidism (which increases the ratio of estrogen to progesterone) is a major cause of excessive sodium loss.

The increase of adrenalin caused by salt restriction has many harmful effects, including insomnia. Many old people have noticed that a low sodium diet disturbs their sleep, and that eating their usual amount of salt restores their ability to sleep. The activity of the sympathetic nervous system increases with aging, so salt restriction is exacerbating one of the basic problems of aging. Chronically increased activity of the sympathetic (adrenergic) nervous system contributes to capillary leakage, insulin resistance (with increased free fatty acids in the blood), and degenerative changes in the brain (Griffith and Sutin, 1996).

The flexibility of blood vessels (compliance) is decreased by a low-salt diet, and vascular stiffness caused by over-activity of the sympathetic nervous system is considered to be an important factor in hypertension, especially with aging.

Pregnancy toxemia/preeclampsia involves increased blood pressure and capillary permeability, and an excess of prolactin. Prolactin secretion is increased by serotonin, which is one of the substances increased by salt restriction, but prolactin itself can promote the loss of sodium in the urine (Ibarra, et al., 2005), and contributes to vascular leakage and hypertension.

In pregnancy, estrogen excess or progesterone deficiency is an important factor in the harmful effects of sodium restriction and protein deficiency. A deficiency of protein contributes to hypothyroidism, which is responsible for the relative estrogen excess.

Protein, salt, thyroid, and progesterone happen to be thermogenic, increasing heat production and stabilizing body temperature at a higher level. Prolactin and estrogen lower the temperature set-point.

The downward shift of temperature and energy metabolism in toxemia or salt deprivation tends to slow the use of oxygen, increasing the glycolytic use of sugar, and contributing to the formation of lactic acid, rather than carbon dioxide. In preeclampsia, serum lactate is increased, even while free fatty acids are interfering with the use of glucose.

One way of looking at those facts is to see that a lack of sodium slows metabolism, lowers carbon dioxide production, and creates inflammation, stress and degeneration. Rephrasing it, sodium stimulates energy metabolism, increases carbon dioxide production, and protects against inflammation and other maladaptive stress reactions.

In recent years, Weissman’s “wear-and-tear” theory of aging, and Pearl’s “rate of living” theory have been clearly refuted by metabolic studies that are showing that intensified mitochondrial respiration decreases cellular damage, and supports a longer life-span.

Many dog owners are aware that small dogs eat much more food in proportion to their size than big dogs do. And small dogs have a much greater life expectancy than big dogs, in some cases about twice as long (Speakman, 2003).

Organisms as different as yeasts and rodents show a similar association of metabolic intensity and life-span. A variety of hamster with a 20% higher metabolic rate lived 15% longer than hamsters with an average metabolic rate (Oklejewicz and Daan, 2002).

Individuals within a strain of mice were found to vary considerably in their metabolic rate. The 25% of the mice with the highest rate used 30% more energy (per gram of body weight) than the 25% with the lowest metabolic rate, and lived 36% longer (Speakman, et al., 2000).

The mitochondria of these animals are “uncoupled,” that is, their use of oxygen isn’t directly proportional to the production of ATP. This means that they are producing more carbon dioxide without necessarily producing more ATP, and that even at rest they are using a considerable amount of energy.

One important function of carbon dioxide is to regulate the movement of positively charged alkali metal ions, such as sodium and calcium. When too much calcium enters a cell it activates many enzymes, prevents muscle and nerve cells from relaxing, and ultimately kills the cell. The constant formation of acidic carbon dioxide in the cell allows the cell to remove calcium, along with the small amount of sodium which is constantly entering the cell.

When there is adequate sodium in the extracellular fluid, the continuous inward movement of sodium ions into the resting cell activates an enzyme, sodium-potassium ATPase, causing ATP to break down into ADP and phosphate, which stimulates the consumption of fuel and oxygen to maintain an adequate level of ATP. Increasing the concentration of sodium increases the energy consumption and carbon dioxide production of the cell. The sodium, by increasing carbon dioxide production, protects against the excitatory, toxic effects of the intracellular calcium.

Hypertonic solutions, containing more than the normal concentration of sodium (from about twice normal to 8 or 10 times normal) are being used to rescuscitate people and animals after injury. Rather than just increasing blood volume to restore circulation, the hypertonic sodium restores cellular energy production, increasing oxygen consumption and heat production while reducing free radical production, improves the contraction and relaxation of the heart muscle, and reduces inflammation, vascular permeability, and edema.

Seawater, which is hypertonic to our tissues, has often been used for treating wounds, and much more concentrated salt solutions have been found effective for accelerating wound healing (Mangete, et al., 1993).

There have been several publications suggesting that increasing the amount of salt in the diet might cause stomach cancer, because countries such as Japan with a high salt intake have a high incidence of stomach cancer.

Studies in which animals were fed popular Japanese foods--“salted cuttlefish guts, broiled, salted, dried sardines, pickled radish, and soy sauce”--besides a chemical carcinogen, showed that the Japanese foods increased the number of tumors. But another study, adding only soy sauce (with a salt content of about 18%) to the diet did not increase the incidence of cancer, in another it was protective against stomach cancer (Benjamin, et al., 1991). Several studies show that dried fish and pickled vegetables are carcinogenic, probably because of the oxidized fats, and other chemical changes, and fungal contamination, which are likely to be worse without the salt. Animals fed dried fish were found to have mutagenic urine, apparently as a result of toxic materials occurring in various preserved foods (Fong, et al., 1979).

Although preserved foods develop many peculiar toxins, even fresh fish in the diet have been found to be associated with increased cancer risk (Phukan, et al., 2006).

When small animals were given a milliliter of a saturated salt solution with the carcinogen, the number of tumors was increased with the salt. However, when the salt was given with mucin, it had no cancer promoting effect. Since the large amount of a saturated salt solution breaks down the stomach’s protective mucus coating, the stomach cells were not protected from the carcinogen. Rather than showing that salt causes stomach cancer, the experiments showed that a cup or more of saturated salt solution, or several ounces of pure salt, shouldn’t be ingested at the same time as a strong carcinogen.

Some studies have found pork to be associated with cancer of the esophagous (Nagai, et al., 1982), thyroid (Markaki, et al., 2003), and other organs, but an experiment with beef, chicken, or bacon diet in rats provides another perspective on the role of salt in carcinogenesis. After being given a carcinogen, rats were fed meat diets, containing either 30% or 60% of freeze-dried fried beef, chicken, or bacon. Neither beef nor chicken changed the incidence of precancerous lesions in the intestine, but the incidence was reduced by 12% in the animals on the 30% bacon diet, and by 20% in rats getting the diet with 60% bacon. Salt apparently made the difference.

Other protective effects of increased sodium are that it improves immunity (Junger, et al., 1994), reduces vascular leakiness, and alleviates inflammation (Cara, et al., 1988). All of these effects would tend to protect against the degenerative diseases, including tumors, atherosclerosis, and Alzheimer’s disease. The RAA system appears to be crucially involved in all kinds of sickness and degeneration, but the protective effects of sodium are more basic than just helping to prevent activation of that system.

A slight decrease in temperature can promote inflammation (Matsui, et al., 2006). The thermogenic substances--dietary protein, sodium, sucrose, thyroid and progesterone--are antiinflammatory for many reasons, but very likely the increased temperature itself is important.

A poor reaction to stress, with increased cortisol, can raise the body temperature by accelerating the breakdown and resynthesis of proteins, but adaptive resistance to stress increases the temperature by increasing the consumption of oxygen and fuel. In the presence of increased cortisol, abdominal fat increases, along with circulating fatty acids and calcium, as mitochondrial respiration is suppressed.

When mice are chilled, they spontaneously prefer slightly salty water, rather than fresh, and it increases their heat production (Dejima, et al., 1996). When rats are given 0.9 per cent sodium chloride solution with their regular food, their heat production increases, and their body fat, including abdominal fat, decreases (Bryant, et al., 1984). These responses to increased dietary sodium are immediate. Part of the effect of sodium involves regulatory processes in the brain, which are sensitive to the ratio between sodium and calcium. Decreasing sodium, or increasing calcium, causes the body’s metabolism to shift away from thermogenesis and accelerated respiration.

Regulating intracellular calcium by increasing the production of carbon dioxide is probably a basic mechanism in sodium’s protection against inflammation and excitatory cell damage and degeneration.

Cortisol’s suppression of mitochondrial respiration is closely associated with its ability to increase intracellular calcium. Cortisol blocks the thermogenic effects of sodium, allowing intracellular calcium to damage cells. With aging, the tissues are more susceptible to these processes.

The thermogenic effects of sodium can be seen in long-term studies, as well as short. A low-sodium diet accelerates the decrease in heat production that normally occurs with aging, lowering the metabolic rate of brown fat and body temperature, and increasing the fat content of the body, as well as the activity of the fat synthesizing enzyme (Xavier, et al., 2003).

Activation of heat production and increased body temperature might account for some of the GABA-like sedative effects of increased sodium. Increasing GABA in the brain increases brown fat heat production (Horton, et al., 1988). Activation of heat production by brown fat increases slow wave sleep (Dewasmes, et al., 2003), the loss of which is characteristic of aging. (In adult humans, the skeletal muscles have heat-producing functions similar to brown fat.)

Now that inflammation is recognized as having a central role in the degenerative diseases, the fact that renin, angiotensin, and aldosterone all contribute to inflammation and are increased by a sodium deficiency, should arouse interest in exploring the therapeutic uses of sodium supplementation, and the integrated use of all of the factors that normally support respiratory energy production, especially thyroid and progesterone. Progesterone’s antagonism to aldosterone has been known for many years, and the synthetic antialdosterone drugs are simply poor imitations of progesterone.

But the drug industry is interested in selling new drugs to block the formation and action of each of the components of the RAAS, rather than an inexpensive method (such as nutrition) to normalize the system.

bonnieh

Posted by @bonnieh, May 12, 2012

sorry no recent updates had computer difficulties. finally got the computer back to running, no more loaner computer, look for updates in a day or two folks!

bonnieh

Posted by @bonnieh, May 13, 2012

Hypervolemic hyponatremia - both sodium & water content increase, but the water gain is greater

cirrhosis
congestive heart failure
nephrotic syndrome
massive edema of any cause

bonnieh

Posted by @bonnieh, May 13, 2012

HYPONATREMIA CAUSES: An abnormally low plasma sodium level is best considered in conjunction with the person's plasma osmolality and extracellular fluid volume status. Indeed, correct ascertainment of volume status, as well as determination of the presence or absence of edema, are both critical in establishing the cause of hyponatremia. As described above, a state of volume depletion leads to increased blood levels of ADH and thus water retention.

The greater the amount of water that is retained, the more the blood sodium will become diluted to cause worsening degrees of hyponatremia. The presence of edema indicates that blood volume has been lost insofar as fluid from the blood has shifted out into the peripheral tissues to cause the edema. In other words, edema is usually reflecting a state of blood volume depletion. As a result, edematous states are also associated with increased blood levels of ADH, water retention, and hyponatremia. In all cases of volume depletion-associated hyponatremia, it is important to note that retention of water ''per se'', such as that promoted by ADH, does not correct the volume depleted state.

In addition to volume depletion, there are other causes of increased ADH levels (and ultimately, therefore, of hyponatremia). These include nausea, pain, and opiate drugs such as codeine and morphine. Such factors often play a role in the hyponatremia that is frequently seen in hospitalized patients.

bonnieh

Posted by @bonnieh, May 13, 2012

Sodium plays a vital role in maintaining the concentration and volume of the extracellular fluid (ECF). It is the main cation of the ECF and a major determinant of ECF osmolality. Sodium is important in maintaining irritability and conduction of nerve and muscle tissue and assists with the regulation of acid-base balance. The average daily intake far exceeds the normal daily requirements. The kidneys are responsible for excreting the excess and are capable of conserving sodium during periods of extreme sodium restriction. The kidneys accomplish this primarily through regulation of water intake/excretion. If the serum sodium falls, the kidneys respond by excreting water. If the serum sodium increases (increased osmolality)---thirst center is stimulated--increased ADH release by the posterior pituitary---acts on kidney to conserve water. Aldosterone also plays a key role by regulating Na+/ECF volume. Its release causes the kidneys to conserve water and sodium which results in increased ECF volume. Because changes in serum sodium levels typically reflect changes in body water balance, gains or losses of total body sodium are not necessarily reflected by the serum sodium level.
Hyponatremia: (Serum sodium less than 136 meq/L)
Clinical indicators and treatment depend on the cause of hyponatremia and whether or not it is associated with a normal, decreased or increased ECF volume.
Signs and symptoms: neurologic symptoms usually do not occur until the serum sodium level has dropped to approximately 120-125 meq/L. Hyponatremia with decreased ECF volume: irritability, apprehension, dizziness, postural hypotension, dry mucus membranes, cold and clammy skin, tremors, seizures. Hyponatremia with normal or increased ECF volume: headache, lassitude, apathy, confusion, weakness, edema, weight gain, elevated blood pressure, muscle cramps, convulsions.
History and risk factors: diarrhea, fistulas, vomiting, NG suction, diuretics, adrenal insufficiency, skin losses (burns, wound drainage), other. Note: hyperlipidemia, hyperproteinemia, and hyperglycemia may cause a pseudo-hyponatremia. This must be ruled out before determining therapy. For every 100 mg/dl increase in glucose, the sodium is diluted by 1.6 meq/L.
Diagnostic tests: serum sodium will be less than 136 meq/L. Serum osmolality will be decreased except in cases of pseudo-hyponatremia, azotemia, or toxins that increase osmolality (example: ethanol). Urine specific gravity will be decreased because of the kidneys attempt to excrete excess water. Urine sodium: decreased (except in SIADH and adrenal insufficiency).
Collaborative management: The goal of therapy is to get the patient out of immediate danger (eg return the sodium level to greater than 120 meq/L) and then gradually return the serum sodium to a normal level and restore normal ECF volume.

bonnieh

Posted by @bonnieh, May 13, 2012

Hyponatremia is an important electrolyte abnormality with the potential for significant morbidity and mortality. Common causes include medications and the syndrome of inappropriate antidiuretic hormone (SIADH) secretion. Hyponatremia can be classified according to the volume status of the patient as hypovolemic, hypervolemic, or euvolemic. Hypervolemic hyponatremia may be caused by congestive heart failure, liver cirrhosis, and renal disease. Differentiating between euvolemia and hypovolemia can be clinically difficult, but a useful investigative aid is measurement of plasma osmolality. Hyponatremia with a high plasma osmolality is caused by hyperglycemia, while a normal plasma osmolality indicates pseudohyponatremia or the post-transurethral prostatic resection syndrome. The urinary sodium concentration helps in diagnosing patients with low plasma osmolality. High urinary sodium concentration in the presence of low plasma osmolality can be caused by renal disorders, endocrine deficiencies, reset osmostat syndrome, SIADH, and medications. Low urinary sodium concentration is caused by severe burns, gastrointestinal losses, and acute water overload. Management includes instituting immediate treatment in patients with acute severe hyponatremia because of the risk of cerebral edema and hyponatremic encephalopathy. In patients with chronic hyponatremia, fluid restriction is the mainstay of treatment, with demeclocycline therapy reserved for use in persistent cases. Rapid correction should be avoided to reduce the risk of central pontine myelinolysis. Loop diuretics are useful in managing edematous hyponatremic states and chronic SIADH. In all instances, identifying the cause of hyponatremia remains an integral part of the treatment plan.

bonnieh

Posted by @bonnieh, May 13, 2012

SODIUM METABOLISM

1. Extracellular fluid contains about 3000 mEq of sodium, which is the main osmotic component. An increase or decrease as small as 1% of the total extracellular fluid volume can have serious effects. About 30,000 mEq of sodium undergo filtration at the glomeruli each day.
2. Several factors are active in the regulation of sodium in the body.
a. Renin is the enzyme responsible for the conversion of antiotensinogen to angiotensin I. An angiotensin converting enzyme converts angiotensin I to angiotensin II. Angiotensin causes vasoconstriction as well as the secretion of aldosterone from the adrenal gland. Renal hypoperfusion, adrenaline and other catecholamines stimulate renin secretion from the juxtaglomerular apparatus of the glomeruli.
b. Aldosterone is a hormone that is controlled by the renin-angiotensin system and acts to increase reabsorption of sodium in the cortical collecting duct.
c. Dopamine from the kidney inhibits reabsorption in the proximal tubules.
d. Prostaglandins block reabsorption in the tubules and stimulate renal vasodilatation.
e. Atrial natriuretic peptide blocks reabsorption of sodium in the collecting duct.

HYPONATREMIA
Definition:
1 Hyponatremia is sodium level under 135 mEq/ml but is actually an excess of water
with no effect from the amount of total body sodium.
2 Hypotonicity is always associated with hyponatremia, whereas hyponatremia can be hyper-, iso- or hypotonic.
3 Hypertonic hyponatremia is caused by osmotically active particles in the extracellular fluid (such as glucose) and a shift of water from intracellular to extracellular fluid as a result. Thus, low serum sodium is accompanied by normal or high osmolality.
4 Isotonic hyponatremia is also called pseudohyponatremia since it is an artifact caused by high lipid or protein in the serum.
5 True hyponatremia is hypotonic with sodium is under 125 mEq/ml and serum osmolality under 250 Osm/kg.
6 Hyponatremia can further be divided into hypovolemic states (GI, renal or third-space losses), isovolemic states and hypervolemic states (CHF, nephrotic syndrome, cirrhosis).
Etiology:
1 Increased fluid intake – more than 1000 ml/hour is more than the body is able to excrete and so water concentration exceeds sodium concentration. This is seen in psychiatric patients with water intoxication or in patients given hypotonic fluids intravenously in large amounts. This is isovolemic hyponatremia.
2 Decreased excretion of water
a. Increased reabsorption in the proximal tubules may reduce the kidney’s ability to excrete water. This can be caused by hypoperfusion due to hypovolemia, or disease states such as congestive heart failure, cirrhosis, or nephrotic syndrome (hypervolemia). The urine is low in sodium, due to increased reabsorption also of sodium. BUN is high.
b. A GFR that falls to less than 10% of normal reflects a decrease in the kidney’s ability to deal with water excretion.
c. Increased reabsorption in the collecting tubules is caused by ADH secretion that is not osmotically stimulated. Urine sodium is normal, with high urine osmolality.
3 SIADH (syndrome of inappropriate ADH secretion) is non-osmotically induced and connected with various disorders of the CNS (tumors, trauma, psychiatric disturbances) and of the lungs (oat cell carcinoma, infection, bronchospastic disease). It is also seen with hypopituarism due to primary adrenal insufficiency or impaired ACTH secretion, and with various drugs, particularly chlorpropamide, clofibrate, carbamazepine, and thiazide diuretics. Idiopathic SIADH may occur in the elderly and is probably connected to increasing ADH secretion with age. One type of SIADH, called “reset osmostat” is seen in patients with chronic illness or malnutrition. The set point for sodium concentration is lowered and the body maintains that value. SIADH is isovolemic.
Manifestations:
1 Depend on the underlying problem.
2 Hyponatremia may cause edema of brain tissues. Acute hyponatremia may cause acute CNS dysfunction with obtundation, coma, seizures and even death. Prolonged hyponatremia may cause permanent CNS damage due to edema of brain cells.

Diagnosis:
1. Plasma is hypotonic and urine osmolality is more than 50-100 Osm/kg.
2. Urine sodium is high in SIADH, but low with edema or hypovolemic states.
3. Water loading test – the patient is given 20ml/kg of water over 20-40 minutes. 80% of this should be excreted within 4 hours with urine osmolality below 100 Osm/kg afterward. If not, the kidney’s ability to excrete water is impaired.

Principles of management:
1 The first step is to reduce fluid intake to about 700 ml/day.
2 The giving of hypertonic infusions such as 3% sodium chloride will increase tonicity of the extracellular fluid. Serum sodium concentration should be increased slowly, no more than 2 mEq/hr. Too rapid correction may cause central pontine myelinolysis. Since rapid volume expansion may cause pulmonary edema, usually a diuretic such as furosemide is given at the same time. The goal is to reach a serum sodium level of 125 mEq/ml. Further correction to normal values can be done more slowly. The formula used is:

(125 – current Na level) x total body water (which equals body weight x 0.6) = mEq of hypertonic saline needed

3 Furosemide given with saline will increase water excretion transiently.
4 Demeclocycline acts on ADH-controlled movement of water in the collecting tubule. Dose is 600-1200 mg/day and several days are required to show an effect. This drug should not be used in patients with kidney disease, heart failure or liver disease.

Prognosis:
1. Acute hyponatremia can cause increased intracranial pressure and brain
damage.
2. Chronic hyponatremia may have a permanent effect on cognitive functions – the theory is controversial.



HYPERNATREMIA

Definition:
1. Hypernatremia is clinically significant above 155 mEq/ml.
2. Hypernatremia is always hypertonic.

Etiology
1. Renal causes
a. Decreased effect of ADH
(1) central diabetes insipidus – failure of secretion or synthesis of ADH due to tumor, trauma, sarcoidosis or histiocytosis
(2) nephrogenic diabetes insipidus – high levels of ADH with no effect, due to renal disease, sickle cell anemia, urinary tract obstruction, hypercalcemia, hypokalemia, lithium or demeclocycline use.
b. Osmotic diuresis as in hyperglycemia – both water and sodium reabsorption are affected, but water losses are more than sodium losses.

2. Extrarenal causes
a. Reduced fluid intake – the body loses water through urine and feces, as well as insensible losses via the skin and mucus membranes. A minimum of about 700 ml/day is necessary in cool climates, more in warmer areas.
b. Vomiting and diarrhea increase gastrointestinal losses.
c. Sweating and burns increase losses via the skin.

Manifestations:
1 Most of the volume decrease is in intracellular fluid, but there is also a slight decrease in extracellular fluid.
2 Urine volume is reduced in cases of extrarenal water losses and normal kidney function. Polyuria is seen with renal causes.
3 Young children and the elderly may show CNS depression with obtundation, coma or seizures. Intracranial or subarachnoid hemorrhages may result from the tearing of bridging veins as brain volume decreases.

Diagnosis
1. Water deprivation test – the patient is given no fluids from 20:00 for 14 hours at which point urine osmolality is tested. It should be greater than 800 Osm/kg. An injection of 5 units ADH is then given which normally does not further increase osmolality. ADH deficiency is suspected if osmolality does not reach 800 after 14 hours or increases by more than 15% after ADH is injected. With nephrogenic diabetes insipidus, the osmolality will be less than 300 with no increase after ADH injection.
2. Urine osmolality under 150 Osm/L is characteristic of a primary problem of water conservation. Urine osmolality over 150 Osm/L with polyuria is characteristic of osmotic diuresis.
3. Urinary concentrations of sodium, glucose and urea may help to determine etiology. Bicarbonate diuresis manifests with a urine pH exceeding 6.
4. Actual ADH levels may need to be assayed in plasma since urine osmolality does not reflect ADH levels in nephrogenic diabetes insipidus.

Principles of management:
1 Fluids, either intravenous as 5% dextrose or orally as water, should be given. Hemolysis may result if fluids given are hypotonic less than 150 Osm/L.
2 Thiazide diuretics reduce polyuria by stimulating reabsorption of sodium and water in the proximal tubule. They are effective in nephrogenic diabetes insipidus.
3 ADH or vasopressin may be given as a nasal spray, 10-20 mg every 12 hours.
4 Drugs that cause SIADH may be useful.

Complications: only if access to water is limited

bonnieh

Posted by @bonnieh, May 25, 2012

Hyponatremia is an important electrolyte abnormality with the potential for significant morbidity and mortality. Common causes include medications and the syndrome of inappropriate antidiuretic hormone (SIADH) secretion. Hyponatremia can be classified according to the volume status of the patient as hypovolemic, hypervolemic, or euvolemic. Hypervolemic hyponatremia may be caused by congestive heart failure, liver cirrhosis, and renal disease. Differentiating between euvolemia and hypovolemia can be clinically difficult, but a useful investigative aid is measurement of plasma osmolality. Hyponatremia with a high plasma osmolality is caused by hyperglycemia, while a normal plasma osmolality indicates pseudohyponatremia or the post-transurethral prostatic resection syndrome. The urinary sodium concentration helps in diagnosing patients with low plasma osmolality. High urinary sodium concentration in the presence of low plasma osmolality can be caused by renal disorders, endocrine deficiencies, reset osmostat syndrome, SIADH, and medications. Low urinary sodium concentration is caused by severe burns, gastrointestinal losses, and acute water overload. Management includes instituting immediate treatment in patients with acute severe hyponatremia because of the risk of cerebral edema and hyponatremic encephalopathy. In patients with chronic hyponatremia, fluid restriction is the mainstay of treatment, with demeclocycline therapy reserved for use in persistent cases. Rapid correction should be avoided to reduce the risk of central pontine myelinolysis. Loop diuretics are useful in managing edematous hyponatremic states and chronic SIADH. In all instances, identifying the cause of hyponatremia remains an integral part of the treatment plan.

Hyponatremia generally is defined as a plasma sodium level of less than 135 mEq per L (135 mmol per L). This electrolyte imbalance is encountered commonly in hospital and ambulatory settings.The results of one prevalence study in a nursing home population demonstrated that 18 percent of the residents were in a hyponatremic state, and 53 percent had experienced at least one episode of hyponatremia in the previous 12 months. Acute or symptomatic hyponatremia can lead to significant rates of morbidity and mortality. Mortality rates as high as 17.9 percent have been quoted, but rates this extreme usually occur in the context of hospitalized patients. Morbidity also can result from rapid correction of hyponatremia. Because there are many causes of hyponatremia and the treatment differs according to the cause, a logical and efficient approach to the evaluation and management of patients with hyponatremia is imperative.

Water and Sodium Balance

Plasma osmolality, a major determinant of total body water homeostasis, is measured by the number of solute particles present in 1 kg of plasma. It is calculated in mmol per L by using this formula:

2 × [sodium] + [urea] + [glucose]

Total body sodium is primarily extracellular, and any increase results in increased tonicity, which stimulates the thirst center and arginine vasopressin secretion. Arginine vasopressin then acts on the V2 receptors in the renal tubules, causing increased water reabsorption. The opposite occurs with decreased extracellular sodium: a decrease inhibits the thirst center and arginine vasopressin secretion, resulting in diuresis. In most cases, hyponatremia results when the elimination of total body water decreases. The pathophysiology of hyponatremia will be discussed later in this article.

Clinical Signs and Symptoms

Most patients with hyponatremia are asymptomatic. Symptoms do not usually appear until the plasma sodium level drops below 120 mEq per L (120 mmol per L) and usually are nonspecific (e.g., headache, lethargy, nausea).In cases of severe hyponatremia, neurologic and gastrointestinal symptoms predominate.3 The risk of seizures and coma increases as the sodium level decreases. The development of clinical signs and symptoms also depends on the rapidity with which the plasma sodium level decreases. In the event of a rapid decrease, the patient can be symptomatic even with a plasma sodium level above 120 mEq per L. Poor prognostic factors for severe hyponatremia in hospitalized patients include the presence of symptoms, sepsis, and respiratory failure.

Diagnostic Strategy

Figure 113 shows an algorithm for the assessment of hyponatremia. The identification of hyponatremia must be followed by a clinical assessment of the patient, beginning with a targeted history to elicit the symptoms of hyponatremia and exclude important causes such as congestive heart failure, liver or renal impairment, malignancy, hypothyroidism, Addison’s disease, gastrointestinal losses, psychiatric illness, recent drug ingestion, surgery, or reception of intravenous fluids. The patient then should be classified into one of the following categories: hypervolemic (edematous), hypovolemic (volume depleted), or euvolemic.

Assessment of Hyponatremia

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FIGURE 1

HYPERVOLEMIC HYPONATREMIA

Hyponatremia in the presence of edema indicates increased total body sodium and water. This increase in total body water is greater than the total body sodium level, resulting in edema. The three main causes of hypervolemic hyponatremia are congestive heart failure, liver cirrhosis, and renal diseases such as renal failure and nephrotic syndrome. These disorders usually are obvious from the clinical history and physical examination alone.

EUVOLEMIC AND HYPOVOLEMIC HYPONATREMIA

Hyponatremia in a volume-depleted patient is caused by a deficit in total body sodium and total body water, with a disproportionately greater sodium loss, whereas in euvolemic hyponatremia, the total body sodium level is normal or near normal. Differentiating between hypovolemia and euvolemia may be clinically difficult, especially if the classic features of volume depletion such as postural hypotension and tachycardia are absent.

Laboratory markers of hypovolemia, such as a raised hematocrit level and blood urea nitrogen (BUN)-to-creatinine ratio of more than 20, may not be present. In fact, results of one study showed an increased BUN-to-creatinine ratio in only 68 percent of hypovolemic patients. Two useful aids for evaluating euvolemic or hypovolemic patients are measurement of plasma osmolality and urinary sodium concentration. Plasma osmolality testing places the patient into one of three categories, normal, high, or low plasma osmolality, while urinary sodium concentration testing is used to refine the diagnosis in patients who have a low plasma osmolality.

Plasma Osmolality Measurement

NORMAL PLASMA OSMOLALITY

The combination of hyponatremia and normal plasma osmolality (280 to 300 mOsm per kg [280 to 300 mmol per kg]) of water can be caused by pseudohyponatremia or by the post-transurethral prostatic resection syndrome. The phenomenon of pseudohyponatremia is explained by the increased percentage of large molecular particles, such as proteins and fats in the serum, relative to sodium. These large molecules do not contribute to plasma osmolality, resulting in a state in which the relative sodium concentration is decreased, but the overall osmolality remains unchanged. Severe hypertriglyceridemia and hyperproteinemia are two causes of this condition in patients with pseudohyponatremia. These patients usually are euvolemic.

The post-transurethral prostatic resection syndrome consists of hyponatremia with possible neurologic deficits and cardiorespiratory compromise. Although the syndrome has been attributed to the absorption of large volumes of hypotonic irrigation fluid intraoperatively, its pathophysiology and management remain controversial.

INCREASED PLASMA OSMOLALITY

Increased plasma osmolality (more than 300 mOsm per kg of water) in a patient with hyponatremia is caused by severe hyperglycemia, such as that occurring with diabetic ketoacidosis or a hyperglycemic hyperosmolar state. It is caused by the presence of glucose molecules that exert an osmotic force and draw water from the intracellular compartment into the plasma, with a diluting effect. Osmotic diuresis from glucose then results in hypovolemia. Fortunately, hyperglycemia can be diagnosed easily by measuring the bedside capillary blood glucose level.

DECREASED PLASMA OSMOLALITY

Patients with low plasma osmolality (less than 280 mOsm per kg of water) can be hypovolemic or euvolemic. The level of urine sodium is used to further refine the differential diagnosis.

High Urine Sodium Level

Excess renal sodium loss can be confirmed by finding a high urinary sodium concentration (more than 30 mmol per L). In these patients, the main causes of hyponatremia are renal disorders, endocrine deficiencies, reset osmostat syndrome, syndrome of inappropriate antidiuretic hormone secretion (SIADH), and drugs or medications. Because of their prevalence and importance, SIADH and drugs deserve special mention, and the author will elaborate on these causes later in the article.

Renal disorders that cause hyponatremia include sodium-losing nephropathy from chronic renal disease (e.g., polycystic kidney, chronic pyelonephritis) and the hyponatremic hypertensive syndrome that frequently occurs in patients with renal ischemia (e.g., renal artery stenosis or occlusion). The combinations of hypertension plus hypokalemia (renal artery stenosis) or hyperkalemia (renal failure) are useful clues to this syndrome.

Endocrine disorders are uncommon causes of hyponatremia. Diagnosing hypothyroidism or mineralocorticoid deficiency (i.e., Addison’s disease) as a cause of hyponatremia requires a high index of suspicion, because the clinical signs can be quite subtle. In either case, the serum levels of thyroid-stimulating hormone (TSH), cortisol, and adrenocorticotropic hormone (ACTH) should be measured, because hypothyroidism and hypoadrenalism can coexist as a polyendocrine deficiency disorder (i.e., Schmidt’s syndrome). Treatment of Schmidt’s syndrome involves steroid replacement before thyroxine T4 therapy to avoid precipitating an addisonian crisis.

The reset osmostat syndrome occurs when the threshold for antidiuretic hormone secretion is reset downward. Patients with this condition have normal water-load excretion and intact urine-diluting ability after an oral water-loading test. The condition is chronic—but stable—hyponatremia. It can be caused by pregnancy, quadriplegia, malignancy, malnutrition, or any chronic debilitating disease.

Low Urine Sodium Level

Patients with extra-renal sodium loss have a low urinary sodium concentration (less than 30 mmol per L) as the body attempts to conserve sodium. Causes include severe burns and gastrointestinal losses from vomiting or diarrhea. Acute water overload, which usually is obvious from the patient’s history, occurs in patients who have been hydrated rapidly with hypotonic fluids, as well as in psychiatric patients with psychogenic overdrinking.

Diuretic therapy, on the other hand, can cause either a low or a high urinary-sodium concentration, depending on the timing of the last diuretic dose administered, but the presence of concomitant hypokalemia is an important clue to the use of a diuretic.

bonnieh

Posted by @bonnieh, Feb 29, 2012

Bloating with low blood sodium is extremely dangerous.
A potentially very dangerous situation in endurance athletes is low blood sodium. During an ultra event, an athlete may drink plenty of water, but not replace the sodium lost in sweat. If the athlete starts retaining water (bloating), then the decrease of sodium in the body and the increase in fluid will result in a too low concentration of sodium in the blood.
Bloating with low blood sodium is extremely dangerous because it can lead to a potentially fatal brain swelling. Mental changes and/or seizures (convulsions) in a bloated athlete are signs of brain swelling and represent a dire medical emergency.
Low sodium is called hyponatremia. "Hypo-" means too little and "-natremia" means sodium status. Hyponatremia means that the concentration of sodium in blood plasma is too small. If the plasma volume increases, then even if the amount of sodium has not decreased, the concentration of sodium will have decreased.
Bloating means increased water weight. In an exercising athlete, bloating is a red flag suggesting hyponatremia. In some athletes, the kidneys, for reasons that are not understood, fail to increase the rate of urination to dump a moderate fluid overload. The same athletes at rest may properly excrete the fluid overload that caused them to bloat during exercise. It is also possible to ingest more fluid than any kidneys could possibly excrete, for example, a 100 lb athlete consuming two quarts per hour at 80 degrees F and riding at a slow speed.
Be vigilant about bloating. Signs include puffiness (at feet and ankles, watchband, ring, and shorts elastic band), and perhaps a forehead-type of headache, which is aggravated by riding on a bumpy road. The rider begins to feel (and look) like the Michelin Man.
A bloated athlete should not consume water and should not consume any sports drink until the bloat has been urinated. (All sports drinks are too dilute in sodium and will only increase the fluid overload.) Stopping exercise will allow urination to start (the athlete must continue to be closely monitored for signs of brain swelling until he/she has urinated a significant volume).
Oral ingestion of salt may get urination to "kick in". On long rides I monitor the symptoms of bloating and my experience suggests that I can reverse bloating by taking in salt and restricting fluid intake. I am also able, I think, to prevent bloating by topping up on salt proportional to my water intake (~1000 mg sodium per quart water).
The only definitive diagnosis of hyponatremia is a blood test for sodium. Keeping track of weight can tell whether an athlete has bloated (weight increases during the ride), or dehydrated (weight decreases during the ride). Watch also for the signs of bloating described above.
Riders and crews may erroneously view bloating as indicative of too high a sodium concentration (hyper-natremia). Bloating is the opposite of dehydration. In the exercising athlete it suggests an existing or imminent hyponatremia, not hypernatremia. The danger of bloating hyponatremia is greatly increased if it is misdiagnosed as dehydration and treated as such. All fatal and severe cases of hyponatremia reported in the literature have involved bloating.

mindy62

Posted by @mindy62, Mar 22, 2012

I, too, have a sodium deficiency. This is not a condition to mess around with. I first learned of my condition in February 2001 when I became wildly disoriented and erratic while out shopping alone. The store called the police, who took me to the hospital. They discovered my sodium level was 113, and I was later told I would have died had I not gotten to a hospital. I spent a week there as they slowly raised my sodium level. During that time, my mental confusion continued and I had one hallucination after another. The hospital didn't know how to treat me. They had a staff psychiatrist evaluate me, and he diagnosed psychosis and put me on a high dose (5 mg) this anti-psychotic drug called Haldol, which only worsened my mental state. It took me more than three months to recover, during which time I had to be off work without pay. I searched for the next four years for the cause and treatments for my condiiton. Finally, my primary care physician sent me to an endocronologist, who tested me and found the condition was caused by a hormonal issue in my kidneys. My treatment is 0.1 mg of fludrocortisone (generic) a day, plus drinking no more than 1,400 ml (about 5 cups) of liquid a day (this means ANY liquid - water, soda, coffee, etc.) The restriction means I am always thirsty and also prone to dehydration. I just found this site the other day,and I have posted comments looking for anyone who has found alternative treatments that might be more tolerable. Despite the treatment, since March 2011 my sodium has been steadily decreasing. It was 128 the last time I had it checked. I am going back to the endocronologist. I'm afraid she's going to reduce my fluid intake even further. I hate the fluid restriction, but I do it because I know it's required for me to stay healthy and alive. I really urge you to see a specialist (like an endocronologist) to get your condition under control. My doctor says simply eating more salt won't help, since my body has trouble retaining it. The sodium just runs right through my system. I hope I haven't scared you, but I really wanted to stress that this is a serious condition that needs to be resolved. Everybody's different, so you really need to find a doctor who will design a plan for you. Best of luck to you, Bonnie. I really hope you find someone who can help.

bonnieh

Posted by @bonnieh, Dec 20, 2012

The body maintains a careful balance of electrolytes like sodium, potassium and chloride within the cells as well as in fluid outside the cells like blood and body fluids. Sodium is necessary to carry out some important functions like maintaining blood pressure. It also helps to maintain the function of nerves and muscles. Sodium enters the body through food and fluid intake. The common salt or table salt contains sodium chloride and it is used not only for cooking but also in preservatives. The same sodium chloride also is the reason for the salinity of our oceans. Excess sodium is excreted by the kidneys via the urine. Sodium levels in the plasma are normally maintained at a level of between 135 to 145 mmol/L.

The condition in which plasma level of sodium falls to below 135 mmol/L is called hyponatremia. Hyponatremia causes movement of excess water in the cells, causing them to swell. The cells of the brain in particular are unable to cope up with this swelling since they are confined within the bones of the skull. Thus, many of the symptoms caused by hyponatremia, especially severe cases, are related to the brain.

When taking medication we must remember that some of the drugs cause hyponatremia as a side effect. Many among these bring about this effect by resulting in a condition called SIADH or Syndrome of Inappropriate Secretion of ADH. ADH (antidiuretic hormone) or vasopressin is a hormone secreted by a small gland near the brain called the pituitary. It plays an important role in water absorption from the kidneys and stimulates thirst. Thus, in conditions of dehydration, by increasing water absorption from the urine and stimulating thirst, it helps to maintain the water content of the body.

SIADH is a condition where the control of ADH secretion is lost and it is secreted independent of the need to conserve water. This results in water retention and subsequent dilution of sodium levels, leading to hyponatremia.

Symptoms of hyponatremia may be mild like:

Nausea, vomiting, headache, and muscle cramps, or Symptoms may be serious like alteration in mental status including confusion, seizures and coma.

If hyponatremia is diagnosed, a careful history should be taken from the patients or their caregivers to find out if the patients are taking any medications that could result in hyponatremia. Stopping the medication usually helps to solve the problem.

bonnieh

Posted by @bonnieh, Dec 20, 2012

Drug and Medication Use

Medications and drugs that cause hyponatremia are listed in Table 1. Some of the more common causes of medication-induced hyponatremia are diuretics and selective serotonin reuptake inhibitors (SSRIs). Most of the medications cause SIADH, resulting in euvolemic hyponatremia. Diuretics cause a hypovolemic hyponatremia. Fortunately, in most cases, stopping the offending agent is sufficient to cause spontaneous resolution of the electrolyte imbalance.

TABLE 1
Agents that Cause Hyponatremia
--------------------------------------------------------------------------------
Diuretics

Carbamazepine (Tegretol)

Chlorpromazine (Thorazine)

Vasopressin analogs

Indapamide (Natrilix)

Selective serotonin reuptake inhibitors

Theophylline

Amiodarone (Cordarone)

Ecstasy (3,4-methylenedioxymethamphetamine)

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