Clinical manifestations are primarily neurologic (due to an osmotic shift of water into brain cells causing edema), especially in acute hyponatremia, and include headache, confusion, and stupor; seizures and coma may occur.
Diagnosis is by measuring serum Na. Serum and urine electrolytes and osmolality help determine the cause.
Treatment involves restricting water intake and promoting its loss, replacing any Na deficit, and correcting the underlying cause.
The causes of hyponatremia may vary depending on its type.
Hyponatremia is classified into three types:
Hypervolemic hyponatremia: In this case, both sodium and water content increase. Increase in the amount of sodium leads to hypervolemia and water content to hyponatremia. The body has independent regulatory mechanisms for both these processes.
Euvolemic hyponatremia: Expansion of volume occurs in the body. There is no edema but hyponatremia occurs.
Hypovolemic hyponatremia: The hypovolemia is due to extracellular volume loss which in turn is due to sodium loss. The hyponatremia is caused by a relatively smaller loss in total body water
These are conditions in which the total body sodium level is truly normal and the sodium blood level is artificially low. Treatment is directed at the etiology of lab artifact, not specifically the sodium level.
Hyperglycemia: The sodium level is decreased by 1.6 meq/l for every 100 mg/dl increase in glucose above normal. The high glucose load causes a transcellular shift of water out of the cell into the vascular space unaccompanied by sodium. This drops the serum sodium level. Mannitol and sorbitol can do the same.
Hyperlipedemia: In this case, there is normal sodium level and this is simply a lab artifact.
Depending on types, the causes of hypovolemia are:
Miscellaneous causes of hyponatremia that are not included under the above classification scheme include the following:
factitious hyponatremia (due to massive increases in blood triglyceride levels, extreme elevation of immunoglobulins as may occur in multiple myeloma, and very high level of blood glucose)
Hypothyroidism and adrenal insufficiency (both thyroid hormone and cortisol are required to excrete free water)
Beer potomania and other malnourished states where poor dietary protein intake leads to inadequate urine solute formation thereby impeding the kidney's ability to excrete free water
Primary polydipsia (where the amount of urine solute required to excrete huge quantities of ingested water exceeds the body's ability to produce it; this typically occurs when 12 or more liters of water are ingested per day)
A prolonged period of exercise may be a cause.
4 Making a Diagnosis
Because the signs and symptoms of hyponatremia occur in many conditions, it's impossible to diagnose the condition based on a physical exam alone.
The approach to the patient with hyponatraemia involves using a combination of clinical assessment and measurements of serum osmolality and urinary sodium.
The cause is often apparent from the history and examination, but other conditions can only be diagnosed with the use of targeted investigations. The most common cause is syndrome of inappropriate antidiuretic hormone secretion (SIADH). However this is a diagnosis of exclusion.
Cerebral salt-wasting syndrome produces a hypovolaemic clinical picture, with a high urine output and normal or low urine osmolality. By contrast, SIADH produces a euvolaemic clinical picture with a low urine output and increased urine osmolality. However, there are no clearly defined thresholds, and controversy exists as to whether the distinction between these 2 conditions is possible or meaningful.
A rapid decline in serum sodium levels over 24 to 48 hours can lead to severe cerebral edema and CNS symptoms including
This is an acute medical emergency. If no acute intervention is initiated to increase sodium level, patients can develop coma, brainstem herniation, and respiratory arrest, leading to death.
A slower decline in sodium levels over several days or weeks is usually asymptomatic; when it is symptomatic, it produces milder cerebral edema, which does not lead to brainstem herniation.
Establishing the type of hyponatraemia
The first step is to measure effective serum osmolality (tonicity). If it is normal, the patient has pseudohyponatraemia (isotonic hyponatraemia), 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 mmol/kg H2O (>295 mOsm/kg H2O), the patient has redistributive hyponatraemia (hypertonic), which is either due to hyperglycaemia or to the absorption or administration of a hypertonic fluid (e.g., mannitol, glycine, or sorbitol).
Hyperglycaemia is usually caused by diabetes but can also be caused by medications (beta-blockers, thiazide diuretics, corticosteroids, nicotinic acid, pentamidine, protease inhibitors, and some antipsychotics) or by stress from a recent stroke, myocardial infarction, trauma, infection, or inflammation. A fasting or random serum glucose measurement establishes hyperglycaemia as the cause. The serum HbA1c is elevated in people with poorly controlled diabetes and may also be useful. Medication-induced hyponatraemia and hyperglycaemia should resolve once the causative agent is discontinued.
Hypertonic hyponatraemia 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. A difference of >10 indicates the presence of non-sodium effective osmoles such as mannitol, glycine, or sorbitol.
If the serum osmolality is <280 mmol/kg H2O (<280 mOsm/kg H2O), the patient has hypotonic hyponatraemia (hypovolaemic, euvolaemic, or hypervolaemic).
Patients with hypovolaemic hyponatraemia will have signs of volume depletion (decreased skin turgor, reduced jugular venous pressure, decreased blood pressure).
Patients with hypervolaemic hyponatraemia will have an elevated jugular venous pressure and peripheral oedema.
The absence of any of these signs indicates that the patient is euvolaemic.
Because hyponatraemia can arise in hypervolaemic, euvolaemic, and hypovolaemic states, hyponatraemia and its cause may not initially be clear.The most important test to identify the aetiology in patients with hypovolaemic hypotonic hyponatraemia, euvolaemic hypotonic hyponatraemia, or hypervolaemic hypotonic hyponatraemia 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.
Hypervolaemic hyponatraemia: urinary sodium >20 mmol/L (>20 mEq/L) suggests chronic renal failure and a urinary sodium ≤20 mmol/L (20 mEq/L) suggests oedematous disorders such as heart failure, cirrhosis, or nephrotic syndrome.
Patients with euvolaemic hyponatraemia always have a urinary sodium >20 mmol/L (>20 mEq/L).
It is also important to measure urine osmolality. Urine osmolality is <100 mmol/kg H2O (<100 mOsm/kg H2O) in cases of excessive water intake, but >100 mmol/kg H2O (>100 mOsm/kg H2O) in all other causes. Differences in urine osmolality between SIADH and cerebral salt-wasting syndrome may be helpful in distinguishing these conditions. However, in general, urine osmolality is measured primarily to assess disease severity and is not useful for elucidating the underlying cause. It should be noted that causes such as endocrinopathies (glucocorticoid deficiency), potassium depletion, and diuretic use may present with either a euvolaemic or hypovolaemic state depending on the severity of the disease.
Hypovolaemic hyponatraemia with urinary sodium >20 mmol/L (>20 mEq/L)
The hyponatraemia may appear within days or even years of starting the medication, and will resolve once thiazide diuretics have been discontinued.
Salt-wasting nephropathy should be considered as a cause in all patients with hypovolaemic hyponatraemia with a urinary sodium >20 mmol/L (>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 haematuria 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.
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 euvolaemic hyponatraemia 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.
Should also be excluded as a cause. Symptoms and signs are usually non-specific 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.
Hypovolaemic hyponatraemia with urinary sodium ≤20 mmol/L (≤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. Hypervolaemic hyponatraemia with urinary sodium ≤20 mmol/L (≤20 mEq/L) Congestive heart failure
A history of myocardial infarction should prompt consideration of congestive heart failure. Symptoms include fatigue, decreased exercise tolerance, dyspnoea on exertion, orthopnoea, and paroxysmal nocturnal dyspnoea. Clinical signs include oedema, displaced cardiac apex, hepatojugular reflux, jugular venous distension, S3 gallop, pulmonary rales, and hepatomegaly.
Chest x-ray may show cardiomegaly, pulmonary oedema, 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.
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 hypervolaemic hyponatraemia is usually symptomatic. Symptoms include fatigue, weakness, weight gain, and pruritus. Signs include oedema, 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.
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 non-steroidal anti-inflammatory drugs, and, very rarely, interferon-alpha, lithium, heroin, mercury, or formaldehyde). Patients present with leg or generalised oedema and foamy urine. Patients may also have Muehrcke's lines (due to hypoalbuminaemia) or xanthelasmas (due to hypertriglyceridaemia).
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.
Hypervolaemic hyponatraemia with urinary sodium >20 mmol/L (>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 haematuria 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.
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 mmol/kg H2O (<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 >6 litres of beer a day on a background of chronic poor dietary intake. Urine osmolality is <100 mmol/kg H2O (<100 mOsm/kg H2O). Serum bilirubin levels are typically elevated and AST and ALT are rarely >200 units/L.
A transient increase in ADH secretion occurs during this period. The hyponatraemia is self-limiting. However, administration of hypotonic fluids during this time can produce a more severe or prolonged hyponatraemia.
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 euvolaemic hypotonic hyponatraemia.
Large volumes of hypotonic fluids are used to irrigate the operative field during endometrial ablation. If absorbed, this can produce severe acute hyponatraemia.
If all other causes of euvolaemic hyponatraemia have been excluded, the patient has SIADH.
Known drug causes include vasopressin, non-steroidal anti-inflammatory drugs, nicotine, chlorpropamide, carbamazepine, tricyclic antidepressants, SSRIs, vincristine, thioridazine, cyclophosphamide, clofibrate, and ecstasy use.
Recent head injury, intracranial surgery, subarachnoid haemorrhage, stroke, brain tumours, 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 tumours 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, leukaemia, and pancreatic cancer.
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.
Treatment methods for hyponatremia may vary depending on its types.
Mild hyponatremia should resolve with fluid restriction. Mild refers to the absence of symptoms, not a specified level.
Moderate hyponatremia can be managed with normal saline administration combined with a loop diuretic, such as a furosemide. The saline gives sodium, and the diuretic causes a net free water loss.
Severe hyponatremia such as that resulting in a seizure or coma should be managed with 3% hypertonic saline or the V2 receptor antagonists conivaptan and tolvaptan. It would be unusual to see severe symptoms with a sodium level greater than 120.
The rate of rise of sodium level should be monitored so as not to cause central pontine myelinolysis. This is what happens if the sodium level is corrected too rapidly. Generally, the rate of rise should not exceed 0.5-1.0 meq/hr. This means no more than 12 point rise in a 12-24 hour period. Hyponatremia can be corrected as rapidly as 2meq/hr if the patient is seizing and the matter is extremely urgent. Fludrocortisone is used for cerebral salt wasting syndrome.
You can prevent hyponatremia by closely monitoring your health in times of sickness such as diarrhea.
If intravenous sodium solution is prescribed to rise the blood sodium level, care must be taken not to administer too much of the solution too quickly. Rapid administration of sodium can increase the risk of a neurological condition developing called central pontine myelinolysis. The treatment is administered in a way that does not allow the blood sodium level to rise by more than 8 mmol/l every 24 hours.
The use of hypotonic fluids such as 5% glucose or sodium chloride 0.18% with glucose 4% and sodium chloride 0.45% should be routinely checked to avoid any risk of dilutional hyponatremia developing.
The patient’s blood levels of urea and electrolytes (sodium, potassium, magnesium, calcium and phosphates) should be routinely monitored. Their blood and urine osmolality should also be checked.
Fluid balance charts should be maintained regularly and accurately to detect hyponatremia and fluid overload.
Associated conditions such as adrenal gland insufficiency should be treated appropriately and adequately to avoid hyponatremia.
Healthcare staff should be aware of the hyponatremia risk associated with the use of certain medications such as diuretics.
Athletes should closely monitor their water intake. Athletes should drink enough fluid to replace the fluid lost during training but should also be careful not to drink so much fluid that they increase their risk for hyponatremia. For heavy training sessions, drinks containing electrolytes may be preferred to replenish the sodium and reduce the risk of hyponatremia.
Indicators that can help judge a patient’s water intake include their thirst level and the color of their urine. If they are not thirsty and their urine is pale yellow in color, they are well hydrated and the water intake has been adequate.
7 Lifestyle and Coping
Lifestyle modifications are necessary in order to cope with hyponatremia.
Include naturally high sodium foods. Some foods naturally contain more sodium than others. Including more of these foods can help maintain a higher sodium balance.
Try including one or more servings of these high sodium foods daily: fish and shellfish, swiss chard and spinach, artichokes, seaweed, red meat, and eggs.
Also include foods that are high in salt and have other benefits. For example fermented foods like sauerkraut or kimchi have higher sodium contents but also have been shown to be beneficial for digestion.
Do not consume a lot of highly refined or high processed foods. Even though these are typically higher in sodium, they also come with a cost of being higher in sugar, fat and calories. You want to manage sodium levels in the healthiest way possible.
Add salt to your foods and cooking. Another easy way to get in extra sodium to your diet is by using more salt on your meals and while you cook.
One teaspoon of salt contains about 2300-2500 mg of sodium. Sprinkle your meals with a little salt and use it while you're cooking.
When using prepared sauces, marinades or canned foods, do not choose low-sodium items. Also try using products that contain higher salt contents. For example: use salted butter instead of unsalted butter.
Avoid caffeine and alcohol. These categories of fluids may worsen low sodium levels. Both can cause electrolyte imbalances and also act as a mild diuretic.
Caffeinated drinks to avoid include: coffee, tea and energy drinks. Be sure to look for bottled juices or sports drinks that promise an "increase in energy" as they might also contain caffeine.
Although it's appropriate to consume alcohol occasionally, it should be completely avoided if you are suffering from low sodium levels and are having difficulty managing them.
Restrict your water intake. Cutting back on the amount of water and other clear fluids you consume can help manage sodium levels. Too much water can dilute the sodium levels in your blood and make them more difficult to manage.
Although water is crucial to your health, you shouldn't over consume it. In general your thirst should guide you to what is an appropriate amount of fluid. If you're not thirsty, you're most likely consuming an adequate amount of fluid.
Also take note of your urine color. If your urine is pale yellow and you're using the bathroom between 4-6 times daily, you're most likely consuming adequate fluids daily.
Reducing your water intake will help your body naturally raise its ratio of sodium to water. This may be easier and more effective than sodium replacement.
Drink sports drinks. These drinks contain electrolytes and will provide the necessary amount of minerals, including sodium.
Even the low calorie or diet sports drinks contain extra sodium and other helpful electrolytes.
Sports drinks are also a great way to replenish temporarily reduced sodium levels after vigorous exercise.
Drink oral rehydrating solutions (ORS) to boost sodium in case of excessive fluid loss. Oral rehydrating solutions are especially helpful in cases of diarrhea, vomiting, and excessive sweating.
Commercially-available ORS can be bought over the counter. They are usually meant to be diluted with 1 L of water and consumed in one sitting.
ORS can also be made at home using 6 level teaspoons of sugar and 3/4 teaspoon of salt, diluted in 1 quart of water. You can mix this solution with powdered flavorings to help make the solution more palatable.
Coconut water is also a good ORS substitute as it contains natural electrolytes to help manage fluid balance.
Talk to your physician. If you're dealing with low sodium levels or is having difficulty managing them with lifestyle and dietary changes, it's important to speak with your doctor. They will be able to tell you how to appropriately and safely manage your condition.
Your doctor may prescribe different medications to help manage your low sodium levels. Always follow these directions prior to making any dietary or other lifestyle changes.
Ask your physician if there are changes you can make at home to help support a normal sodium level.
Take anti-nausea medication. If your low sodium level is due to vomiting, you may want to consider trying an over-the-counter anti-nausea medicine. Taking anti-nausea medicine to make sure that you stop the excessive loss of fluid due to vomiting.
When you vomit, you expel most of the contents of your stomach, including water, sodium and other electrolytes.
If you are vomiting excessively, such as during a stomach flu or other bacterial illness, you may lose so much water and sodium that your sodium levels drop dangerously low.
In addition to anti-nausea medications, you may also want to consider natural ways to manage nausea and vomiting. Ginger tea, ginger soda and more small frequent meals can help reduce nausea and vomiting.
Always talk to your doctor prior to taking any over-the-counter medications.
Take anti-diarrheals. Another common cause of low sodium levels is diarrhea. Taking an over-the-counter medication to help lessen or stop diarrhea can help you manage low sodium levels.
Diarrhea causes your body to flush out a large amount of fluids. It doesn’t have the time to absorb the needed minerals, including sodium.
Take anti-diarrheal medications to stop diarrhea and allow your body time to reestablish your sodium levels.
In addition to medication, there are some natural ways to manage diarrhea. Try including bland, non-fibrous foods like bananas, white rice and toast. Also avoid high fibrous foods and dairy as these can make diarrhea worse.
Consult with your personal physician prior to taking any over the counter medications.
8 Risks and Complications
Hyponatremia or a low blood sodium level is associated with several complications. In cases of chronic or long-term hyponatremia, the level of sodium in the blood drops gradually over days or weeks symptoms may therefore develop gradually and be of moderate severity.
In cases of acute hyponatremia on the other hand, the risk of developing potentially life-threatening complications is higher. The symptoms develop rapidly, over a very short period of time and may lead to a medical emergency. For example, acute hyponatremia can cause the brain to swell. This is a particularly dangerous condition called cerebral edema that can lead to coma and death within a matter of hours if left untreated.
Brain damage caused by hyponatremia appears to pose a greater risk among premenopausal women, possibly due to the influence of female sex hormones on the body’s ability to regulate sodium levels. Some of the complications associated with hyponatremia are described below:
Chronic hyponatremia can lead to neurological complications that affect a person’s gait or walk as well as their ability to pay attention. Together, these effects lead to a reduced reaction time and an increased susceptibility to falls and injuries. Hyponatremia may also lead to the development of osteoporosis, which can increase the risk of bone fracture. One study showed that the odds of developing osteoporosis were almost three times greater among adults who had mild hyponatremia than among those who had normal blood sodium levels.
Acute hyponatremia can lead to much more severe complications such as cerebral edema, brain disease, herniation of the brain, cardiopulmonary arrest, seizure, coma and even death.
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