|
|
Click on any of the headings or subheadings to rapidly navigate to the relevant section of the guidemap
Risk factors for developing hyponatremia
Medical decision-making and treatment
| Introduction |
- hyponatremia is defined as a serum sodium < 135 meq/L and hyponatremia usually implies a state of hypotonicity with a relative excess of body water compared to sodium
- however, hyponatremia does not necessarily imply that the total body water is absolutely increased and the patient may be clinically hypovolemic, euvolemic, or hypervolemic
- a hyponatremic patient, who is clinically hypovolemic, has a decreased total body water and decreased total body sodium, and the patient is hyponatremic (hypotonic) because the depleted body fluids have been partially replaced with relatively hypotonic fluids (eg. tap water or soft drinks po, hyponatremic oral pediatric formulaes or hypotonic saline/dextrose IV solutions) causing a relative excess of water compared to sodium
- a hyponatremic patient, who is clinically hypervolemic, usually has an increased total body sodium + an increased total body water, and the patient is hyponatremic (hypotonic) because there is greater degree of free water retention compared to the amount of sodium retention
(* hypervolemic patients with CHF and cirrhosis have an increased total body sodium and total body water due to decreased renal perfusion and secondary hyperaldosteronism, but they may also become hyponatremic because the decreased "effective" blood volume and "functional" underfilling of their arterial circulation => stimulates vasopressin secretion => secondary water retention - overriding the negative feedback effect of the body's osmoreceptors that normally act to decrease vasopressin secretion in response to hyponatremia; while hypervolemic patients with renal failure have a limited ability to excrete their daily water load +/- increased water intake)
- a hyponatremic patient, who is clinically euvolemic, actually has an excess of total body water due to a state of inappropriate ADH secretion or due to an inappropriate sensitivity of the kidney tubules to vasopressin (SIADH), or due to impaired free water clearance +/- excessive water intake; the excess total body water may not be clinically apparent because it is mainly intracellular, and only partly extracellular
(* excess water intake due to voluntary polydipsia or potomania (excessive beer ingestion) rarely causes significant hyponatremia because the normal kidney has a marked ability to excrete dilute urine - suspect an additional/superadded problem preventing the urine from being maximally dilute eg. drug-induced SIADH, concomitant diuretic use or vomiting causing secondary vasopressin secretion, an associated physical illness/stress causing increased vasopressin secretion, or an impaired ability to excrete free water due to an associated glucocorticoid/thyroid hormone deficiency)
- the likelihood of symptomatic hyponatremia depends partly on the magnitude of the hyponatremia (patients are rarely symptomatic if the serum sodium is > 120 meq/L), but it is mainly affected by the rapidity of development of the hyponatremia (symptomatic hyponatremia is much more likely if hyponatremia develops acutely in < 48 hours)
- the brain is the organ most sensitive to hyponatremia and it usually responds to hyponatremia by slowly secreting idiogenic osmoles out of the brain cells into the ECF => it normally takes a few days for the brain cells to accomodate to the hypotonic state by secreting a sufficient amount of idiogenic osmoles to ensure iso-osmolality relative to the ECF
- acute hyponatremia may overwhelm the brain's slow adaptive responses => water passes from the hypotonic ECF space into the brain cells causing cerebral edema (altered LOC and/or seizures) => secondary increased ICP because the rigidity of the skull limits the brain's capacity to expand => clinical signs of increased ICP (altered LOC and/or focal neurological signs and/or respiratory arrest)
(* risk factors for the development of acute cerebral edema include:- postoperative mentruant females, elderly females recently placed on thiazide diuretics, children, psychiatric patients with psychogenic polydipsia and hypoxic patients)
- the opposite phenomenon occurs if chronic hyponatremia is rapidly corrected => the brain takes a few days to regenerate intra-cellular idiogenic osmoles, and water passes from the brain cells into the ECF if the tonicity of the ECF is increased too fast => brain cell dehydration => osmotic demyelination syndrome (formerly called central pontine myelinolysis - usually manifests with mutism, dysphasia, spastic quadriparesis and pseudobulbar palsy a few days later)
| Clinical presentation |
- the clinical signs of mild hyponatremia are often vague and non-specific - anorexia/nausea, muscle cramps, lassitude - and their presence may signify that the hyponatremia is of acute onset
- central nervous symptoms predominate in acute-severe hyponatremia
- lethargy/apathy
- disorientation
- agitation/delirium
- seizures
- obtundation/coma
- cerebral herniation and respiratory arrest
| Risk factors for developing hyponatremia |
| Hypertonic hyponatremia (serum osmolality
> 295 mOsm/L)
Hyperglycemia
|
| Isotonic hyponatremia (serum osmolality
275 - 295 mOsm/L)
Hyperlipidemia
|
| Hypotonic hyponatremia (serum osmolality
< 275 mOsm/L)
Hypovolemic (dehydrated) patients Renal losses (urinary sodium > 20 meq/L)
Urinary sodium > 20 meq/L
Urinary sodium < 10 meq/L
|
| Medical decision-making and treatment |
The initial therapeutic approach to the hyponatremic patient is primarily dictated by the presence of severe hyponatremic symptoms, which is often directly related to a rapid rate of fall of the serum sodium (> 0.5 meq/L/ hour) rather than being directly related to the magnitude of the fall in the serum sodium level
(* acute hyponatremia is actually uncommon and mainly occurs in post-operative patients who receive an excess of IV hypotonic fluid, or in patients with psychogenic polydipsia)
- severe hyponatremic symptoms include seizures, coma and focal neurological signs, and permanent brain damage and death can ensue if acute hyponatremia is not rapidly corrected
- conversely, the absence of symptoms in a hyponatremic patient with severe hyponatremia (serum sodium < 120 meq/L) suggests chronic hyponatremia (> 48 hours old), and patients with chronic hyponatremia are at risk of developing osmotic demyelination syndrome if the serum sodium is corrected too rapidly => in other words, there is more risk of brain damage from the therapy of chronic hyponatremia than from the hyponatremia itself
- therefore, the first decision that has to be made is whether immediate osmotherapy therapy with hypertonic saline is actually necessary - by assessing the extent of any neurological symptoms + the magnitude of the hyponatremia + the rate of development of the hyponatremia (acuteness of onset)
Immediate osmotherapy with hypertonic saline is indicated if the patient has severe symptoms of hyponatremia (seizures, coma +/- signs of herniation) + serum sodium < 120 meq/L + acute hyponatremia
(* acute symptomatic hyponatremia is uncommon in patients with hypervolemic hyponatremia and hypertonic saline administration can induce pulmonary edema in hypervolemic patients => only use hypertonic saline if absolutely necessary + a diuresis should first be induced with a loop diuretic before administering hypertonic saline; acute symptomatic hyponatremia is also uncommon in patients with hypovolemic hyponatremia and most of those patients only require IV fluid replacement with normal saline)
- if the patient is actively seizing or has signs of a markedly increased ICP, hypertonic 3% saline solution should initially be administered at a rate of 3 - 4 cc/kg/hour for 30 - 60 minutes (which usually causes a serum sodium increase of 4 - 6 meq/L/hour) => follow-up with hypertonic saline at 1 - 2 cc/kg/hour prn + measure the serum sodium hourly at first, and then every 2 - 3 hours
- a lower initial dose of hypertonic saline (1 - 2 ml/kg/hour) is recommended if the patient has severe neurological symptoms (confusion or lethargy), but is not actively seizing or herniating
- try to avoid using high doses of hypertonic saline for more than a few hours, because it only takes a ~ 5% increase in the serum sodium to substantially reduce the magnitude of cerebral edema
- try to avoid increasing the serum sodium > 1 - 2 meq/hour for more than a few hours after the immediate (first one-hour) corrective phase of therapy => then lower the hypertonic saline infusion rate to < 0.5cc/kg/hour to prevent the serum sodium concentration from increasing faster than 0.5 meq/L/hour
- try to limit the total daily increase in the serum sodium to < 12 meq/24 hours
- aim for a maximum final serum sodium concentration of 120 meq/L in the first 24 hours
(* a furosemide-induced diuresis is roughly equivalent to 0.5 normal isotonic saline solution and helps eliminate the excess amount of free water)
- there is little practical value to using complicated theoretical formulas to pre-calculate the patient's excess volume of total body free water and a theoretical sodium deficit in the ED setting => it is probably easier to monitor the therapeutic adequacy of hypertonic saline therapy by constantly evaluating the patient's clinical status + measuring the serum sodium concentration every 1 - 2 hours + constantly assessing the urinary output +/- urinary sodium concentration
If the patient is asymptomatic or minimally symptomatic, or if the serum sodium is > 120 meq/L => osmotherapy is not indicated and the emphasis should be targeted toward correcting the underlying condition
- before instituting "targeted" therapy, first exclude:-
- laboratory error
- pseudophyponatremia due to hyperlipidemia or hyperproteinemia
- pseudohyponatremia due to blood sampling proximal to an IV infusion of hypotonic fluid
- redistributive hyponatremia due to hyperglycemia or mannitol
- serum osmolality 280 - 295 mOsm/L => suggests pseudohyponatremia
- serum osmolality > 295 mOsm/L => suggests redistributive hyponatremia
- hypovolemia hyponatremia
- euvolemia hyponatremia
- hypervolemia hyponatremia
- if the patient is hypovolemic + no life-threatening hyponatremic CNS symptoms, the major emphasis should be on restoring the ECF volume and ensuring adequate organ perfusion => normal saline is first used to restore the plasma volume => give 10 - 20cc/kg IV boluses of normal saline until the patient is hemodynamically stable => then administer normal saline at ~ 200cc/hour in the average-sized adult (3cc/kg/hour) to replace the ECF sodium/fluid deficit over 24 hours (optimally 50% of the calculated deficit should be replaced in the first 8 hours, and 50% of the calculated deficit in the next 16 hours) + treat the cause of the hypovolemia
(* hypovolemia is not always readily detectable and mild dehydration may not be clinically apparent => the patient may be incorrectly perceived as having euvolemic hyponatremia and incorrectly treated with water restriction; 1/2 normal saline may have to be used after the initial recuscitative phase if the hyponatremia is over-correcting too fast - limit the rise in serum sodium concentration to < 0.5 meq/L/hour during the first 24 hours)
Euvolemic hyponatremia
- if the patient is euvolemic + no life-threatening hyponatremic CNS symptoms => simple water restriction is the mainstay of initial therapy +/- thyroid hormone or glucocorticoid replacement therapy prn if an associated endocrine deficiency exists
(* additional long-term therapy will often be required in SIADH; while simple interdiction of water intake should correct the problem in psychogenic polydipsia)
Hypervolemic hyponatremia
- if the patient is hypervolemic + no life-threatening hyponatremic CNS symptoms => water restriction + loop diuretic + treat the underlying cause
(* the hyponatremia will often be resistant to treatment unless renal perfusion is increased and vasopressin secretion suppressed - by treating any CHF and increasing forward cardiac output, or by definitive therapy such as dialysis for renal failure, or by organ transplantation for liver failure)
- the complication of osmotic demyelination syndrome is more common in chronic hyponatremia - especially when underlying risk factors are present (alcoholic and/or malnourished and/or hypokalemic patients; pre-menopausal females and children)
- osmotic demyelination syndrome is probably secondary to a too rapid correction of the hyponatremia in a patient already chronically adapted to the hyponatremia => slowly correct the hyponatremia to a maximum serum sodium concentration of 130 meq/L over 48 - 72 hours to decrease the risk of osmotic demyelination syndrome
Diagnostic evaluation of hyponatremia
- the diagnostic evaluation of the hyponatremia can be simply based on the "risk factors for developing hyponatremia" table or the algorithm for diagnosing the cause of the hyponatremia
- => first check that the patient truly has hypotonic hyponatremia by checking that the serum osmolality is < 280 mOsm/L
- = > determine the volume status of the patient
- => check the list of causes of hyponatremia in that volume-status category
- => measure a spot urine sodium concentration if the cause is not clinically obvious after checking the list of causes of hypovolemic hyponatremia and hypervolemic hyponatremia
- => check the urine osmolality to differentiate SIADH from primary polydipsia and other causes of pure water overload in patients with euvolemic hyponatremia
Clinical pearls
- dehydration + hyponatremia + hyperkalemia => adrenal insufficiency (until proven otherwise)
- the commonest cause of hyponatremia in adult ED patients is diuretic use +/- a low-salt diet in a CHF patient, and the type of hypotonic hyponatremia depends on the degree of fluid intake relative to the degree of diuresis - excessive diuresis + inadequate fluid intake => hypovolemic hyponatremia; moderate diuresis + low salt intake + adequate water intake => euvolemic hyponatremia
- a CHF patient taking diuretics may also have hypervolemic hyponatremia due to a worsening cardiac output and only a careful physical examination can differentiate hypervolemic hyponatremia (look for pulmonary edema, peripheral edema, ascites and/or a pleural effusion) from euvolemic hyponatremia
- dehydrated patients are usually thirsty and they strive to maintain their plasma volume by drinking fluids => their degree of hypovolemic hyponatremia depends on the quantity and rate of solute-free water intake
- measure the urinary sodium + plasma and urinary osmolality if the cause of the hyponatremia is not clinically apparent in an euvolemic patient - an inappropriately high urinary sodium and urinary osmolality may suggest SIADH
- suspect glucocorticoid or thyroid hormone deficiency if the patient has euvolemic hyponatremia and there is no underlying disease/drug that may be causing SIADH
| Appendix |
The diagnosis is primarily a disease of exclusion and consists of the following six criteria:-
- hypotonic hyponatremia
- inappropriately elevated urine osmolality (> 200 mosm/L)
- elevated urinary sodium (> 20 meq/L)
- clinical euvolemia + subclinical increased total body water
- normal adrenal, renal, cardiac, hepatic and thyroid function
- correctable with water restriction
| Some causes of SIADH |
Drugs
|
Algorithm for the diagnosis of the cause of the hyponatremia
Disclaimer: My EM guidemaps reflect my personal approach to problem-solving/managing clinical cases in an ED setting and they should not be regarded as the standard of care. They merely represent the personal opinions of the author and they should only be used in clinical practice if the reader-user has substantial reason to believe that the clinical advice contained in the guidemaps is valid and accurate. The guidemaps are not meant to be "authoritative" and the reader-user should consult standard medical textbooks and expert opinion articles/guidelines for more authoritative advice. The reader-user should particularly confirm all drug doses, their indications and contra-indications, prior to their use.