Clinical Slide Set. Hyponatremia

© Copyright Annals of Internal Medicine, 2015Ann Int Med. 163 (3): ITC3-1.

* For Best Viewing:

Open in Slide Show Mode Click on icon or

From the View menu, select the Slide Show option

* To help you as you prepare a talk, we have included the relevant text from ITC in the notes pages of each slide


Terms of Use The In the Clinic® slide sets are owned and copyrighted by the

American College of Physicians (ACP). All text, graphics, trademarks, and other intellectual property incorporated into the slide sets remain the sole and exclusive property of ACP. The slide sets may be used only by the person who downloads or purchases them and only for the purpose of presenting them during not-for-profit educational activities. Users may incorporate the entire slide set or selected individual slides into their own teaching presentations but may not alter the content of the slides in any way or remove the ACP copyright notice. Users may make print copies for use as hand-outs for the audience the user is personally addressing but may not otherwise reproduce or distribute the slides by any means or media, including but not limited to sending them as e-mail attachments, posting them on Internet or Intranet sites, publishing them in meeting proceedings, or making them available for sale or distribution in any unauthorized form, without the express written permission of the ACP. Unauthorized use of the In the Clinic slide sets constitutes copyright infringement.


in the clinic

Hyponatremia


What is hyponatremia? Disorder of water balance

Occurs when more water ingested than kidneys can excrete

Ability to excrete a large volume of dilute urine is compromised

Kidney disease

Diuretics

Low protein intake

Presence of arginine vasopressin

Amount of free water excreted is determined by urine volume, sodium, and potassium Free water is excreted if

urinary sodium + potassium < plasma sodium


Who is at risk for hyponatremia? Endurance athletes Institutionalized patients with schizophrenia People who consume large quantities of fluid but little protein People with severe kidney disease Certain drugs (diuretics, particularly thiazide; SSRIs; SNRIs) If posterior pituitary secretes AVP despite low plasma sodium

Hypovolemia or heart or liver disease AVP secretion without osmotic and hemodynamic stimulus

Syndrome of inappropriate antidiuretic hormone secretion Common in hospitalized patients

Hospitalized children receiving hypotonic fluids


What potential measures can prevent or limit the severity of hyponatremia? Encourage runners to drink fluids only when thirsty

Monitor body weight to avoid weight gain during exercise

Check plasma sodium after initiating thiazides, SNRIs, SSRIs

Check 1 to 2 weeks after initiating therapy

Avoid thiazides in persons with high fluid or low protein intake and during acute illness

Measure plasma sodium in hospitalized patients on admission

Treat low sodium based on the underlying cause

Avoid hypotonic fluids and thiazides

Monitor daily in patients with hyponatremia and in those at increased risk


CLINICAL BOTTOM LINE: Prevention... Hyponatremia is common in patients who:

Participate in endurance exercise Receive thiazides, SSRIs, or SNRIs Have congestive heart failure, cirrhosis, or pneumonia Admitted to the ICU Elderly patients

Avoid hypotonic fluids in hospitalized patients at increased risk


What characteristic symptoms or physical findings should alert clinicians to the diagnosis of hyponatremia? Mild hyponatremia

Subtle neurocognitive deficits Deficits improve when plasma sodium is normalized

Moderate hyponatremia Nausea, confusion, headache, vomiting

Severe hyponatremia Delirium; impaired consciousness; seizures Rarely: cardiorespiratory arrest

Consider hyponatremia in the differential diagnosis of patients with osteoporosis, falls, and hip fractures


What conditions should clinicians consider when evaluating patients with hyponatremia?

Major Causes of Hyponatremia Based on Volume Status

Hypovolemia: Extrarenal losses

Vomiting, diarrhea, sweating

Pancreatitis

Small bowel obstruction

Hypovolemia: Renal losses

Diuretics, osmotic diuresis

Cerebral salt wasting, salt-losing nephritis

Addison disease—continued


Hypervolemia

Heart failure

Liver disease with cirrhosis

Nephrotic syndrome

Chronic kidney disease

Euvolemia

Primary polydipsia

Decreased solute excretion

Diuretics

Hypothyroidism

Cortisol deficiency

Syndrome of inappropriate antidiuretic hormone secretion (SIADH)


Essential

Decreased effective osmolality of the extracellular fluid

Inappropriate urinary concentration in presence of decreased effective serum osmolality

Clinical euvolemia, as defined by the absence of signs of hypovolemia or hypervolemia

Absence of urinary sodium conservation when salt and water intake are normal

Absence of other potential causes of euvolemic hypoosmolality: hypothyroidism, hypocortisolism, diuretics

—continued

Criteria for the Diagnosis of SIADH


Supplemental

Plasma uric acid <4 mg/dL

Blood urea nitrogen <10 mg/dL

Fractional sodium excretion >1%; fractional urea excretion >55%

Abnormal water load test

Plasma AVP level inappropriately elevated relative to plasma osmolality

No significant correction of plasma sodium with volume expansion but improvement after fluid restriction


Common Causes of SIADHTumors

Pulmonary/mediastinal (e.g., small cell carcinoma)

Other cancers (e.g., duodenal, stomach, pancreatic, bladder)

Lymphoma

Ewing sarcoma

Central nervous system disorders

Mass lesions (e.g., tumors, brain abscesses)

Inflammatory diseases (e.g., encephalitis, meningitis)

Degenerative or demyelinating diseases

Miscellaneous: subarachnoid hemorrhage, head trauma, psychosis, delirium tremens, pituitary stalk section, transsphenoidal adenomectomy, hydrocephalus, cerebrovascular accident, cavernous sinus thrombosis

—continued


Drug-induced

Stimulated AVP release (narcotics, nicotine, phenothiazines)

Direct renal effects or potentiation of AVP antidiuretic effects (desmopressin, oxytocin, prostaglandin synthesis inhibitors)

Mixed/uncertain actions (carbamazepine, chlorpropamide, SSRI, clofibrate, clozapine, cyclophosphamide, ecstasy, vincristine)

Pulmonary diseases

Infections

Mechanical or ventilatory (e.g., acute respiratory failure, asthma)

Other

Rocky Mountain spotted fever

AIDS and AIDS-related complex

Nausea, pain, stress, prolonged strenuous exercise

Mutations of the aquaretic vasopressin receptor Idiopathic


What is the overall approach to the diagnosis of hyponatremia?

Initial evaluation

Measure plasma osmolality, glucose, urea, creatinine, and potassium

Measure urine osmolality, sodium, and chloride (if the patient is vomiting)

Base further diagnostic workup on initial evaluation results

Identifying cause of hyponatremia is often difficult


What is the role of volume status, urine osmolality, and urinary sodium in the evaluation of patients with hyponatremia? Measure urine osmolality in hypotonic hyponatremia

<100 mOsm/kg H2O: polydipsia, decreased solute excretion usual cause

<100 mOsm/kg H2O: may also occur after volume resuscitation with hypovolemic hyponatremia (if measured after administration of isotonic saline)

>200 mOsm/kg H2O: AVP playing a role if kidney function normal and patient not receiving diuretics

Determine cause of AVP secretion

Classify volume status based on history and physical: hypovolemia, clinical euvolemia, or hypervolemia

Subdivide hypovolemia: extrarenal or renal sodium losses

—continued


Clinical euvolemia vs. mild hypovolemia

Water retention may make patient seem euvolemic

Hypovolemia: urinary sodium <30 mEq/L

Euvolemia: urinary sodium >30 mEq/L

Hypovolemic hyponatremia vs. SIADH with salt depletion If urinary sodium <20 and >20 mEq/L or <40 mEq/L

Hypovolemic hyponatremia: improves after normal saline

Salt-depleted SIADH: plasma sodium doesn’t normalize after administration of normal saline

Hypervolemia due to HF, cirrhosis, nephrotic syndrome Base diagnosis on history and physical exam

Urinary sodium <30 mEq/L unless on diuretics


What is the role of imaging studies in the diagnosis of hyponatremia?

Chest radiography

Unexplained SIADH: to identify potential underlying cause

Chest computed tomography

Consider for smokers

Magnetic resonance imaging of the brain

If physical exam reveals neurologic abnormalities after plasma sodium is normalized


When should clinicians consult with a nephrologist or endocrinologist?

Cause of hyponatremia is unknown

Guidance for evaluation of SIADH

Guidance on use of normal saline in patients with possible SIADH and plasma sodium levels <120 mEq/L


CLINICAL BOTTOM LINE: Diagnosis... Identifying the cause of hyponatremia can be challenging

Often difficult to distinguish whether patient is slightly volume depleted or euvolemic

If volume status uncertain, saline infusion may be useful Before diagnosing SIADH

Stop thiazides to determine effect on plasma sodium Rule out secondary adrenal insufficiency and

hypothyroidism


What is the overall approach to treatment of hyponatremia? Acute: duration known to be <48 h

Endurance exercise, psychogenic polydipsia, drug use, colonoscopy preparation, and postoperative states

Can lead to cerebral edema with risk for brain herniation

Urgent normalization of sodium levels is needed

Chronic: duration unknown or >48 h

Patients predisposed to brain damage if hyponatremia corrected too rapidly

Hyponatremia severity classification (mEq/L)

U.S.: mild: 130-135, moderate 120-129, severe <120

European: mild 130-135; moderate 125-129, severe <125


How should sodium levels be corrected in acute and severely symptomatic hyponatremia?

Difficult to predict rate of correction of plasma sodium

Acute or severely symptomatic chronic hyponatremia

Rapidly reverse cerebral edema by increasing plasma sodium by 5 mEq/L

Chronic hyponatremia

Do not raise plasma sodium level >10 mEq/L within 24 h and/or >18 mEq/L within 48 h

Set goal of therapy well below therapeutic limit

Recommended rates of correction in patients at high risk for osmotic demyelination: 4-6 mEq/L per day


What is the treatment of patients with chronic asymptomatic hyponatremia?

Hypovolemia due to GI losses and sweating

Isotonic saline; consider concomitant desmopressin

Diuretics

Discontinue; if no improvement administer isotonic saline

Addison disease Isotonic saline; glucocorticoid and mineralocorticoid

replacement

Glucocorticoid insufficiency

Glucocorticoid replacement

—continued


Primary polydipsia Restrict water; discontinue diuretics and any drug known to

cause SIADH If volume-depleted or decreased solute excretion, cautiously

administer isotonic saline and consider desmopressin (if no access to fluids) initially or if rapid increase in urine output and/or plasma sodium

Decreased solute intake

Same treatment as for polydipsia

Additionally: increase electrolytes and protein in the diet

Heart failure

Restrict water, salt; loop diuretics in fluid overload cases

Cirrhosis with ascites

Restrict water and salt; administer diuretics; possible albumin infusion with diuretics

—continued


Nephrotic syndrome Restrict water and salt; diuretics

If clinically decreased effective circulating volume, administer albumin with diuretics

Chronic kidney disease

Restrict water, salt; loop diuretics if fluid overload present

SIADH

Discontinue diuretics and any drug known to cause SIADH

Restrict water but not salt; consider oral urea, salt tablets, furosemide with salt tablets, and demeclocycline if water restriction ineffective

Don’t use vaptans unless benefit is greater than risk and only approved for 1 month of use (FDA guidelines)


What are manifestations of the osmotic demyelination syndrome and who is at risk? If chronic hyponatremia is corrected too rapidly

Brain unable to rapidly recover organic solutes lost in adaptation to hyponatremia

Neurologic symptoms occur 2-6 days after correction

Risk factors

Initial plasma sodium <105 mEq/L; hypokalemia

History of alcoholism, malnutrition, advanced liver disease

Increase in plasma sodium >10 mEq/L within 24 h and >18 mEq/L within 48 h

If cause of hyponatremia reversible, plasma sodium may increase more than intended


When should patients be hospitalized for management of hyponatremia?

Hyponatremic patients who are symptomatic

Confusion, headache, vomiting, and seizures

Acute hyponatremia

Plasma sodium level <125 mEq/L

Risk factors for ODS


How should clinicians counsel patients about salt and fluid intake and when to seek clinical care? Treatment of hypervolemic hyponatremia due to HF

Restrict dietary salt to 1.5 to 3.0 g/day

Restrict fluids to 1.5 to 2 L/day unless hyponatremia worsens

Treatment of SIADH Limit fluids ≈800 mL/day

Do not restrict salt intake

Patients should seek care if they experience altered mental status, falls, or persistent nausea


What other therapies are used in the management of hyponatremia?

Sodium chloride tablets Furosemide (Lasix) Urea Demeclocycline Tolvaptan


If fluid restriction unsuccessful in managing plasma sodium in hyponatremia Concerns about increased risk for rapid correction of plasma

sodium and lack of mortality benefit

Concerns about hepatotoxicity

US FDA: Limit use to 1-month

US FDA: Limit use with plasma sodium <125 mEq/L unless symptomatic + no response to fluid restriction

To avoid overcorrection, use vaptans alone Not in conjunction with other treatment for hyponatremia

Check plasma sodium levels every 6-8 h during initiation and don’t initially restrict fluid intake

When should clinicians consider use of vasopressin-receptor antagonists?


When should clinicians consult a nephrologist or endocrinologist for treatment of hyponatremia?

Considering administration of hypertonic saline or vaptans

Hyponatremia is acute, severe, or symptomatic

Patients have risk factors for ODS

Patients have had overly rapid correction

Patients require long-term therapy


CLINICAL BOTTOM LINE: Treatment... Hospitalization

Patients with acute or severe hyponatremia Patients with moderate to severe symptoms

Acute hyponatremia Administer hypertonic saline to rapidly correct plasma sodium

levels even if asymptomatic Monitor closely Don’t increase >10 mEq/L within 24 h or 18 mEq/L within 48 h Use lower rates of sodium correction in those at risk for ODS Risk factors for ODS Initial plasma sodium level <105 mEq/L Hypokalemia Alcoholism or malnutrition Advanced liver disease

Clinical Slide Set. Hyponatremia

Documents

Transcript of Clinical Slide Set. Hyponatremia