1. HYPONATREMIA WORKSHOPD6
STA. ANA – TANGCO
Dr. Monzon

2. Salient features HISTORY 60 year old female cc: vomiting
Fever, dysuria, frequency
Headache, body malaise, nausea
(-) epigastric pain, diarrhea
(-) smoker and alcohol beverage drinker
(+) HPN on telmisartan 40 mg and hydrocholothiazide 12.5 mg

3. Salient features PHYSICAL EXAMINATION wheel-chair-borne
Orthostatic hypotension
LABORATORY FINDINGS
Presence of infection
Leukocytosis with predominance of neutrophils
Slightly turbid urine
Hyaline cast, Pyuria, Bacteruria
Increased serum creatinine
Decreased serum sodium = hyponatremia

4. GUIDE QUESTIONS

5. HYPOTONIC HYPONATREMIA
1. What is you diagnosis?
HYPOTONIC HYPONATREMIA
a plasma Na+ concentration less than 135 mmol/ L (patient: 123 mmol/L)

6. HYPONATREMIA Pseudo-hyponatremia Hypoosmolal hyponatremia
N plasma osmolality
Hyper-lipidemia
Hyper-proteinuria
↑ plasma osmolality
Hyper-glycemia
Mannitol
Hypoosmolal hyponatremia
1° Na+ loss
Skin loss
GI loss
Renal loss
1° water gain
Hypo-thyroidism
AVP release
SIADH
Chronic renal insufficiency
1° water gain with ° water gain
Heart failure
Hepatic cirrhosis
Nephrotic syndrome

7. 1. What is the basis for your diagnosis?
Infection/ Fever
Vomiting
Nausea
Frequency
Serum Na = 123mmol/L
Orthostatic hypotension
Medications
Neurologic manifestations

8. Basis for diagnosis Vomiting
Results in disturbances in acid-base balance, dehydration and electrolyte depletion
Na+ loss
Infection
fever  sweating  Na+ loss
Frequency
Na+ loss in urine

9. Basis for diagnosis Nausea  ADH   H2O retention  hypoosmolarity
Serum Na+ 123 mmol/L = Hyponatremia
Orthostatic hypotension
Sustained drop in systolic pressure (≥ 20 mmHg) or diastolic pressure (≥ 10 mmHg) within 3 minutes of standing
In nonneurogenic causes (i.e. hypovolemia) the BP drop is accompanied by a compensatory increase in HR (>15bpm)

10. Basis for diagnosis Medications Telmisartan - ARB
 angiotensin II   Na+ reabsorption in tubules  Na + excretion  Na + loss
Hydrochlorothiazide - Diuretic
“diuretics-induced hyponatremia” is almost always due to thiazide diuretics
 Na + reabsorption in tubules  Na + excretion  Na+ loss
** Creatinine levels may increase when ACE inhibitors (ACEI) or angiotensin-II receptor blockers (ARBs)

11. Basis for diagnosis
Neurologic symptoms
Related to osmotic water shift  increased ICF volume (cerebral edema)
Severity is dependent on rate of onset and absolute decrease in plasma Na concentration
As plasma concentration falls…
Nausea, body malaise, headache, lethargy, confusion and obtundation
Plasma concentration < 120 mmol/L
Stupor, seizures, coma

12. 2. What other laboratory tests are needed to be requested for the patient?
4 laboratory findings provide useful information for the diagnosis of hyponatremia
Serum osmolality
Urine osmolality
Urine Na+ concentration
Urine K+ concentration
Serum glucose & lipid profile*
Lab Studies
The diagnosis of hyponatremia depends entirely on the ability to properly obtain a sample of the patient's serum and to accurately measure its concentration of sodium.
When interpreting serum sodium levels, always consider the possibility of sampling error, especially when the reported value does not seem consistent with the history or physical findings.
Was the patient's blood sample properly labeled?
Was it obtained from a venous site proximal to an infusion of hypotonic saline or dextrose in water?
Is laboratory measurement or reporting in error?
If an error is suspected, a second sample should be submitted for testing before therapeutic measures are initiated.
In addition to sampling and analysis errors, several physiologic states exist in which correct laboratory analysis yields low serum sodium levels, but these levels do not reflect a true hypoosmolar state.
The most common example is serum hyperglycemia.
Accumulation of extracellular glucose induces a shift of free water from the intracellular space to the extracellular space.
Serum sodium concentration is diluted by a factor of 1.6 mEq/L for each 100 mg/dL increase above normal serum glucose concentration.
Systemic osmolarity is normal or even increased, not decreased, as in true (ie, hypoosmolar) hyponatremia.
This hypertonic hyponatremia has no physiologic significance, and serum sodium concentration corrects as normoglycemia is reestablished.
A similar phenomenon is observed in patients treated with glycerol or mannitol in an effort to control acute glaucoma or intracranial hypertension. This phenomenon is also seen in patients with advanced renal disease who receive radiocontrast agents for diagnostic testing.
Hyponatremia may be noted in patients whose serum contains unusually large quantities of protein or lipid.
In these patients, an expanded plasma protein or lipid fraction leads to a decrease in the plasma water fraction in which sodium is dissolved.
Laboratory techniques that measure absolute sodium content per unit of plasma water report low sodium levels despite the fact that the concentration of sodium in serum water remains within the normal range.
This phenomenon, known as pseudohyponatremia, occurs when flame emission spectrophotometry or indirect potentiometry is used to assay serum sodium levels rather than direct potentiometry techniques. This occurs in approximately 60% of US laboratories.
Serum osmolarity remains undisturbed, and attempts at correcting serum sodium level are not indicated.
Hyperlipidemia that is severe enough to produce pseudohyponatremia almost always is accompanied by a notably lipemic appearance of the serum sample.
Hyperproteinemia of sufficient magnitude to induce pseudohyponatremia commonly is due to coexisting multiple myeloma.
Serum osmolarity is helpful in establishing the diagnosis of true hypoosmolar hyponatremia. Serum osmolarity is abnormally low in patients with hypoosmolar hyponatremia, but it is normal in patients with pseudohyponatremia due to hyperlipidemia or hyperproteinemia and normal or elevated in patients with hypertonic hyponatremia due to serum hyperglycemia.
Urine sodium levels are helpful in distinguishing renal causes of hyponatremia from nonrenal causes.
Patients with hypovolemic hyponatremia due to nonrenal causes (eg, vomiting, diarrhea, fistulas, GI drainage, third spacing of fluids) have avid renal absorption of tubular sodium and urine sodium levels of less than 20 mEq/L, whereas those with hypovolemic hyponatremia due to renal causes (eg, diuretics, salt-losing nephropathy, aldosterone deficiency) have inappropriately elevated urine sodium levels in excess of 20 mEq/L.
Patients with hypervolemic hyponatremia due to decreases in effective circulating volume (eg, cirrhosis, nephrosis, congestive heart failure) have urine sodium levels of less than 20 mEq/L, whereas those with renal causes of hypervolemic hyponatremia or with SIADH have urine sodium levels in excess of 20 mEq/L.
Urine osmolarity may be helpful in establishing the diagnosis of SIADH.
Typically, patients with SIADH have inappropriately concentrated urine, with urine osmolarities in excess of 100 mOsm/L.
Patients with other forms of hyponatremia and appropriately depressed levels of ADH have urine osmolarities below 100 mOsm/L.
Serum thyroid-stimulating hormone (TSH) and free thyroxine levels should be checked if the clinical presentation is consistent with hypothyroidism.
Adrenal function should be assessed, via random serum cortisol levels or adrenocorticotropic hormone (ACTH) stimulation test, in patients who have recently taken oral steroids or in any patient suspected of having cortisol deficiency.
Imaging Studies
Imaging studies may be indicated depending on the underlying etiology of the hyponatremia (eg, chest radiograph in a patient with congestive heart failure).
Usually, a head CT scan is indicated in the patient with altered mental status to ensure that no other underlying cause for the mental status is present.

13. Plasma Osmolality High Normal Low Hyperglycemia Mannitol
Hyperproteinemia
Hyperlipidemia
Bladder Irrigation
Maximal volume of maximally dilute urine (<100mosmol/kg)
Yes No
Primary polydipsia
Reset osmostat
ECF Volume
Increased
Normal
Decreased
Heart Failure
Hepatic Cirrhosis
Nephrotic Syndrome
Renal Insufficiency
SIADH
Exclude hypothyroidism
Exclude adrenal insufficiency
Urine Na Concentration
>20mmol/L
Na wasting nephropathy
Hypoaldosteronism
Diuretic
Vomiting
<10mmol/L
Extrarenal Na loss
Remote diuretic use
Remote vomiting

14. 2. What other laboratory tests are needed to be requested for the patient?
Serum osmolarity
confirmation of true hypoosmolar hyponatremia
determines fluid status to establish classification of hyponatremia
abnormally low in patients with hypoosmolar hyponatremia
normal or elevated in patients with hypertonic hyponatremia due to serum hyperglycemia.
Lab Studies
The diagnosis of hyponatremia depends entirely on the ability to properly obtain a sample of the patient's serum and to accurately measure its concentration of sodium.
When interpreting serum sodium levels, always consider the possibility of sampling error, especially when the reported value does not seem consistent with the history or physical findings.
Was the patient's blood sample properly labeled?
Was it obtained from a venous site proximal to an infusion of hypotonic saline or dextrose in water?
Is laboratory measurement or reporting in error?
If an error is suspected, a second sample should be submitted for testing before therapeutic measures are initiated.
In addition to sampling and analysis errors, several physiologic states exist in which correct laboratory analysis yields low serum sodium levels, but these levels do not reflect a true hypoosmolar state.
The most common example is serum hyperglycemia.
Accumulation of extracellular glucose induces a shift of free water from the intracellular space to the extracellular space.
Serum sodium concentration is diluted by a factor of 1.6 mEq/L for each 100 mg/dL increase above normal serum glucose concentration.
Systemic osmolarity is normal or even increased, not decreased, as in true (ie, hypoosmolar) hyponatremia.
This hypertonic hyponatremia has no physiologic significance, and serum sodium concentration corrects as normoglycemia is reestablished.
A similar phenomenon is observed in patients treated with glycerol or mannitol in an effort to control acute glaucoma or intracranial hypertension. This phenomenon is also seen in patients with advanced renal disease who receive radiocontrast agents for diagnostic testing.
Hyponatremia may be noted in patients whose serum contains unusually large quantities of protein or lipid.
In these patients, an expanded plasma protein or lipid fraction leads to a decrease in the plasma water fraction in which sodium is dissolved.
Laboratory techniques that measure absolute sodium content per unit of plasma water report low sodium levels despite the fact that the concentration of sodium in serum water remains within the normal range.
This phenomenon, known as pseudohyponatremia, occurs when flame emission spectrophotometry or indirect potentiometry is used to assay serum sodium levels rather than direct potentiometry techniques. This occurs in approximately 60% of US laboratories.
Serum osmolarity remains undisturbed, and attempts at correcting serum sodium level are not indicated.
Hyperlipidemia that is severe enough to produce pseudohyponatremia almost always is accompanied by a notably lipemic appearance of the serum sample.
Hyperproteinemia of sufficient magnitude to induce pseudohyponatremia commonly is due to coexisting multiple myeloma.
Serum osmolarity is helpful in establishing the diagnosis of true hypoosmolar hyponatremia. Serum osmolarity is abnormally low in patients with hypoosmolar hyponatremia, but it is normal in patients with pseudohyponatremia due to hyperlipidemia or hyperproteinemia and normal or elevated in patients with hypertonic hyponatremia due to serum hyperglycemia.
Urine sodium levels are helpful in distinguishing renal causes of hyponatremia from nonrenal causes.
Patients with hypovolemic hyponatremia due to nonrenal causes (eg, vomiting, diarrhea, fistulas, GI drainage, third spacing of fluids) have avid renal absorption of tubular sodium and urine sodium levels of less than 20 mEq/L, whereas those with hypovolemic hyponatremia due to renal causes (eg, diuretics, salt-losing nephropathy, aldosterone deficiency) have inappropriately elevated urine sodium levels in excess of 20 mEq/L.
Patients with hypervolemic hyponatremia due to decreases in effective circulating volume (eg, cirrhosis, nephrosis, congestive heart failure) have urine sodium levels of less than 20 mEq/L, whereas those with renal causes of hypervolemic hyponatremia or with SIADH have urine sodium levels in excess of 20 mEq/L.
Urine osmolarity may be helpful in establishing the diagnosis of SIADH.
Typically, patients with SIADH have inappropriately concentrated urine, with urine osmolarities in excess of 100 mOsm/L.
Patients with other forms of hyponatremia and appropriately depressed levels of ADH have urine osmolarities below 100 mOsm/L.
Serum thyroid-stimulating hormone (TSH) and free thyroxine levels should be checked if the clinical presentation is consistent with hypothyroidism.
Adrenal function should be assessed, via random serum cortisol levels or adrenocorticotropic hormone (ACTH) stimulation test, in patients who have recently taken oral steroids or in any patient suspected of having cortisol deficiency.
Imaging Studies
Imaging studies may be indicated depending on the underlying etiology of the hyponatremia (eg, chest radiograph in a patient with congestive heart failure).
Usually, a head CT scan is indicated in the patient with altered mental status to ensure that no other underlying cause for the mental status is present.

15. Serum osmolarity Normal Range: 280 to 300mOsm/kg
Total osmolality (mOsm)
= 2 (Na + K) + Glucose(mg/dl)/18 + BUN(mg/dl)/2.8
= 2( ) + 98/ /2.8
= 2(126.7) =
 Hypotonic Hyponatremia
Lab Studies
The diagnosis of hyponatremia depends entirely on the ability to properly obtain a sample of the patient's serum and to accurately measure its concentration of sodium.
When interpreting serum sodium levels, always consider the possibility of sampling error, especially when the reported value does not seem consistent with the history or physical findings.
Was the patient's blood sample properly labeled?
Was it obtained from a venous site proximal to an infusion of hypotonic saline or dextrose in water?
Is laboratory measurement or reporting in error?
If an error is suspected, a second sample should be submitted for testing before therapeutic measures are initiated.
In addition to sampling and analysis errors, several physiologic states exist in which correct laboratory analysis yields low serum sodium levels, but these levels do not reflect a true hypoosmolar state.
The most common example is serum hyperglycemia.
Accumulation of extracellular glucose induces a shift of free water from the intracellular space to the extracellular space.
Serum sodium concentration is diluted by a factor of 1.6 mEq/L for each 100 mg/dL increase above normal serum glucose concentration.
Systemic osmolarity is normal or even increased, not decreased, as in true (ie, hypoosmolar) hyponatremia.
This hypertonic hyponatremia has no physiologic significance, and serum sodium concentration corrects as normoglycemia is reestablished.
A similar phenomenon is observed in patients treated with glycerol or mannitol in an effort to control acute glaucoma or intracranial hypertension. This phenomenon is also seen in patients with advanced renal disease who receive radiocontrast agents for diagnostic testing.
Hyponatremia may be noted in patients whose serum contains unusually large quantities of protein or lipid.
In these patients, an expanded plasma protein or lipid fraction leads to a decrease in the plasma water fraction in which sodium is dissolved.
Laboratory techniques that measure absolute sodium content per unit of plasma water report low sodium levels despite the fact that the concentration of sodium in serum water remains within the normal range.
This phenomenon, known as pseudohyponatremia, occurs when flame emission spectrophotometry or indirect potentiometry is used to assay serum sodium levels rather than direct potentiometry techniques. This occurs in approximately 60% of US laboratories.
Serum osmolarity remains undisturbed, and attempts at correcting serum sodium level are not indicated.
Hyperlipidemia that is severe enough to produce pseudohyponatremia almost always is accompanied by a notably lipemic appearance of the serum sample.
Hyperproteinemia of sufficient magnitude to induce pseudohyponatremia commonly is due to coexisting multiple myeloma.
Serum osmolarity is helpful in establishing the diagnosis of true hypoosmolar hyponatremia. Serum osmolarity is abnormally low in patients with hypoosmolar hyponatremia, but it is normal in patients with pseudohyponatremia due to hyperlipidemia or hyperproteinemia and normal or elevated in patients with hypertonic hyponatremia due to serum hyperglycemia.
Urine sodium levels are helpful in distinguishing renal causes of hyponatremia from nonrenal causes.
Patients with hypovolemic hyponatremia due to nonrenal causes (eg, vomiting, diarrhea, fistulas, GI drainage, third spacing of fluids) have avid renal absorption of tubular sodium and urine sodium levels of less than 20 mEq/L, whereas those with hypovolemic hyponatremia due to renal causes (eg, diuretics, salt-losing nephropathy, aldosterone deficiency) have inappropriately elevated urine sodium levels in excess of 20 mEq/L.
Patients with hypervolemic hyponatremia due to decreases in effective circulating volume (eg, cirrhosis, nephrosis, congestive heart failure) have urine sodium levels of less than 20 mEq/L, whereas those with renal causes of hypervolemic hyponatremia or with SIADH have urine sodium levels in excess of 20 mEq/L.
Urine osmolarity may be helpful in establishing the diagnosis of SIADH.
Typically, patients with SIADH have inappropriately concentrated urine, with urine osmolarities in excess of 100 mOsm/L.
Patients with other forms of hyponatremia and appropriately depressed levels of ADH have urine osmolarities below 100 mOsm/L.
Serum thyroid-stimulating hormone (TSH) and free thyroxine levels should be checked if the clinical presentation is consistent with hypothyroidism.
Adrenal function should be assessed, via random serum cortisol levels or adrenocorticotropic hormone (ACTH) stimulation test, in patients who have recently taken oral steroids or in any patient suspected of having cortisol deficiency.
Imaging Studies
Imaging studies may be indicated depending on the underlying etiology of the hyponatremia (eg, chest radiograph in a patient with congestive heart failure).
Usually, a head CT scan is indicated in the patient with altered mental status to ensure that no other underlying cause for the mental status is present.

16. 2. What other laboratory tests are needed to be requested for the patient?
b. Urine osmolality
may be helpful in establishing the diagnosis of SIADH
The appropriate renal response to hypoosmolality is to excrete the maximum volume of dilute urine
Patients with other forms of hyponatremia and appropriately depressed levels of ADH have urine osmolarities below 100 mOsm/L.
Lab Studies
The diagnosis of hyponatremia depends entirely on the ability to properly obtain a sample of the patient's serum and to accurately measure its concentration of sodium.
When interpreting serum sodium levels, always consider the possibility of sampling error, especially when the reported value does not seem consistent with the history or physical findings.
Was the patient's blood sample properly labeled?
Was it obtained from a venous site proximal to an infusion of hypotonic saline or dextrose in water?
Is laboratory measurement or reporting in error?
If an error is suspected, a second sample should be submitted for testing before therapeutic measures are initiated.
In addition to sampling and analysis errors, several physiologic states exist in which correct laboratory analysis yields low serum sodium levels, but these levels do not reflect a true hypoosmolar state.
The most common example is serum hyperglycemia.
Accumulation of extracellular glucose induces a shift of free water from the intracellular space to the extracellular space.
Serum sodium concentration is diluted by a factor of 1.6 mEq/L for each 100 mg/dL increase above normal serum glucose concentration.
Systemic osmolarity is normal or even increased, not decreased, as in true (ie, hypoosmolar) hyponatremia.
This hypertonic hyponatremia has no physiologic significance, and serum sodium concentration corrects as normoglycemia is reestablished.
A similar phenomenon is observed in patients treated with glycerol or mannitol in an effort to control acute glaucoma or intracranial hypertension. This phenomenon is also seen in patients with advanced renal disease who receive radiocontrast agents for diagnostic testing.
Hyponatremia may be noted in patients whose serum contains unusually large quantities of protein or lipid.
In these patients, an expanded plasma protein or lipid fraction leads to a decrease in the plasma water fraction in which sodium is dissolved.
Laboratory techniques that measure absolute sodium content per unit of plasma water report low sodium levels despite the fact that the concentration of sodium in serum water remains within the normal range.
This phenomenon, known as pseudohyponatremia, occurs when flame emission spectrophotometry or indirect potentiometry is used to assay serum sodium levels rather than direct potentiometry techniques. This occurs in approximately 60% of US laboratories.
Serum osmolarity remains undisturbed, and attempts at correcting serum sodium level are not indicated.
Hyperlipidemia that is severe enough to produce pseudohyponatremia almost always is accompanied by a notably lipemic appearance of the serum sample.
Hyperproteinemia of sufficient magnitude to induce pseudohyponatremia commonly is due to coexisting multiple myeloma.
Serum osmolarity is helpful in establishing the diagnosis of true hypoosmolar hyponatremia. Serum osmolarity is abnormally low in patients with hypoosmolar hyponatremia, but it is normal in patients with pseudohyponatremia due to hyperlipidemia or hyperproteinemia and normal or elevated in patients with hypertonic hyponatremia due to serum hyperglycemia.
Urine sodium levels are helpful in distinguishing renal causes of hyponatremia from nonrenal causes.
Patients with hypovolemic hyponatremia due to nonrenal causes (eg, vomiting, diarrhea, fistulas, GI drainage, third spacing of fluids) have avid renal absorption of tubular sodium and urine sodium levels of less than 20 mEq/L, whereas those with hypovolemic hyponatremia due to renal causes (eg, diuretics, salt-losing nephropathy, aldosterone deficiency) have inappropriately elevated urine sodium levels in excess of 20 mEq/L.
Patients with hypervolemic hyponatremia due to decreases in effective circulating volume (eg, cirrhosis, nephrosis, congestive heart failure) have urine sodium levels of less than 20 mEq/L, whereas those with renal causes of hypervolemic hyponatremia or with SIADH have urine sodium levels in excess of 20 mEq/L.
Urine osmolarity may be helpful in establishing the diagnosis of SIADH.
Typically, patients with SIADH have inappropriately concentrated urine, with urine osmolarities in excess of 100 mOsm/L.
Patients with other forms of hyponatremia and appropriately depressed levels of ADH have urine osmolarities below 100 mOsm/L.
Serum thyroid-stimulating hormone (TSH) and free thyroxine levels should be checked if the clinical presentation is consistent with hypothyroidism.
Adrenal function should be assessed, via random serum cortisol levels or adrenocorticotropic hormone (ACTH) stimulation test, in patients who have recently taken oral steroids or in any patient suspected of having cortisol deficiency.
Imaging Studies
Imaging studies may be indicated depending on the underlying etiology of the hyponatremia (eg, chest radiograph in a patient with congestive heart failure).
Usually, a head CT scan is indicated in the patient with altered mental status to ensure that no other underlying cause for the mental status is present.

17. 2. What other laboratory tests are needed to be requested for the patient?
c. Urine Sodium Level
to identify renal from nonrenal causes
If due to nonrenal causes
eg, vomiting, diarrhea, fistulas, GI drainage, third spacing of fluids
have avid renal absorption of tubular sodium and urine sodium levels of less than 20 mEq/L
If due to renal causes
eg, diuretics, salt-losing nephropathy, aldosterone deficiency
have inappropriately elevated urine sodium levels in excess of 20 mEq/L.
Lab Studies
The diagnosis of hyponatremia depends entirely on the ability to properly obtain a sample of the patient's serum and to accurately measure its concentration of sodium.
When interpreting serum sodium levels, always consider the possibility of sampling error, especially when the reported value does not seem consistent with the history or physical findings.
Was the patient's blood sample properly labeled?
Was it obtained from a venous site proximal to an infusion of hypotonic saline or dextrose in water?
Is laboratory measurement or reporting in error?
If an error is suspected, a second sample should be submitted for testing before therapeutic measures are initiated.
In addition to sampling and analysis errors, several physiologic states exist in which correct laboratory analysis yields low serum sodium levels, but these levels do not reflect a true hypoosmolar state.
The most common example is serum hyperglycemia.
Accumulation of extracellular glucose induces a shift of free water from the intracellular space to the extracellular space.
Serum sodium concentration is diluted by a factor of 1.6 mEq/L for each 100 mg/dL increase above normal serum glucose concentration.
Systemic osmolarity is normal or even increased, not decreased, as in true (ie, hypoosmolar) hyponatremia.
This hypertonic hyponatremia has no physiologic significance, and serum sodium concentration corrects as normoglycemia is reestablished.
A similar phenomenon is observed in patients treated with glycerol or mannitol in an effort to control acute glaucoma or intracranial hypertension. This phenomenon is also seen in patients with advanced renal disease who receive radiocontrast agents for diagnostic testing.
Hyponatremia may be noted in patients whose serum contains unusually large quantities of protein or lipid.
In these patients, an expanded plasma protein or lipid fraction leads to a decrease in the plasma water fraction in which sodium is dissolved.
Laboratory techniques that measure absolute sodium content per unit of plasma water report low sodium levels despite the fact that the concentration of sodium in serum water remains within the normal range.
This phenomenon, known as pseudohyponatremia, occurs when flame emission spectrophotometry or indirect potentiometry is used to assay serum sodium levels rather than direct potentiometry techniques. This occurs in approximately 60% of US laboratories.
Serum osmolarity remains undisturbed, and attempts at correcting serum sodium level are not indicated.
Hyperlipidemia that is severe enough to produce pseudohyponatremia almost always is accompanied by a notably lipemic appearance of the serum sample.
Hyperproteinemia of sufficient magnitude to induce pseudohyponatremia commonly is due to coexisting multiple myeloma.
Serum osmolarity is helpful in establishing the diagnosis of true hypoosmolar hyponatremia. Serum osmolarity is abnormally low in patients with hypoosmolar hyponatremia, but it is normal in patients with pseudohyponatremia due to hyperlipidemia or hyperproteinemia and normal or elevated in patients with hypertonic hyponatremia due to serum hyperglycemia.
Urine sodium levels are helpful in distinguishing renal causes of hyponatremia from nonrenal causes.
Patients with hypovolemic hyponatremia due to nonrenal causes (eg, vomiting, diarrhea, fistulas, GI drainage, third spacing of fluids) have avid renal absorption of tubular sodium and urine sodium levels of less than 20 mEq/L, whereas those with hypovolemic hyponatremia due to renal causes (eg, diuretics, salt-losing nephropathy, aldosterone deficiency) have inappropriately elevated urine sodium levels in excess of 20 mEq/L.
Patients with hypervolemic hyponatremia due to decreases in effective circulating volume (eg, cirrhosis, nephrosis, congestive heart failure) have urine sodium levels of less than 20 mEq/L, whereas those with renal causes of hypervolemic hyponatremia or with SIADH have urine sodium levels in excess of 20 mEq/L.
Urine osmolarity may be helpful in establishing the diagnosis of SIADH.
Typically, patients with SIADH have inappropriately concentrated urine, with urine osmolarities in excess of 100 mOsm/L.
Patients with other forms of hyponatremia and appropriately depressed levels of ADH have urine osmolarities below 100 mOsm/L.
Serum thyroid-stimulating hormone (TSH) and free thyroxine levels should be checked if the clinical presentation is consistent with hypothyroidism.
Adrenal function should be assessed, via random serum cortisol levels or adrenocorticotropic hormone (ACTH) stimulation test, in patients who have recently taken oral steroids or in any patient suspected of having cortisol deficiency.
Imaging Studies
Imaging studies may be indicated depending on the underlying etiology of the hyponatremia (eg, chest radiograph in a patient with congestive heart failure).
Usually, a head CT scan is indicated in the patient with altered mental status to ensure that no other underlying cause for the mental status is present.

18. 2. What other laboratory tests are needed to be requested for the patient?
d. Urine Potassium Level
Potassium levels often change with sodium levels
↓ Na+, ↑K+
Lab Studies
The diagnosis of hyponatremia depends entirely on the ability to properly obtain a sample of the patient's serum and to accurately measure its concentration of sodium.
When interpreting serum sodium levels, always consider the possibility of sampling error, especially when the reported value does not seem consistent with the history or physical findings.
Was the patient's blood sample properly labeled?
Was it obtained from a venous site proximal to an infusion of hypotonic saline or dextrose in water?
Is laboratory measurement or reporting in error?
If an error is suspected, a second sample should be submitted for testing before therapeutic measures are initiated.
In addition to sampling and analysis errors, several physiologic states exist in which correct laboratory analysis yields low serum sodium levels, but these levels do not reflect a true hypoosmolar state.
The most common example is serum hyperglycemia.
Accumulation of extracellular glucose induces a shift of free water from the intracellular space to the extracellular space.
Serum sodium concentration is diluted by a factor of 1.6 mEq/L for each 100 mg/dL increase above normal serum glucose concentration.
Systemic osmolarity is normal or even increased, not decreased, as in true (ie, hypoosmolar) hyponatremia.
This hypertonic hyponatremia has no physiologic significance, and serum sodium concentration corrects as normoglycemia is reestablished.
A similar phenomenon is observed in patients treated with glycerol or mannitol in an effort to control acute glaucoma or intracranial hypertension. This phenomenon is also seen in patients with advanced renal disease who receive radiocontrast agents for diagnostic testing.
Hyponatremia may be noted in patients whose serum contains unusually large quantities of protein or lipid.
In these patients, an expanded plasma protein or lipid fraction leads to a decrease in the plasma water fraction in which sodium is dissolved.
Laboratory techniques that measure absolute sodium content per unit of plasma water report low sodium levels despite the fact that the concentration of sodium in serum water remains within the normal range.
This phenomenon, known as pseudohyponatremia, occurs when flame emission spectrophotometry or indirect potentiometry is used to assay serum sodium levels rather than direct potentiometry techniques. This occurs in approximately 60% of US laboratories.
Serum osmolarity remains undisturbed, and attempts at correcting serum sodium level are not indicated.
Hyperlipidemia that is severe enough to produce pseudohyponatremia almost always is accompanied by a notably lipemic appearance of the serum sample.
Hyperproteinemia of sufficient magnitude to induce pseudohyponatremia commonly is due to coexisting multiple myeloma.
Serum osmolarity is helpful in establishing the diagnosis of true hypoosmolar hyponatremia. Serum osmolarity is abnormally low in patients with hypoosmolar hyponatremia, but it is normal in patients with pseudohyponatremia due to hyperlipidemia or hyperproteinemia and normal or elevated in patients with hypertonic hyponatremia due to serum hyperglycemia.
Urine sodium levels are helpful in distinguishing renal causes of hyponatremia from nonrenal causes.
Patients with hypovolemic hyponatremia due to nonrenal causes (eg, vomiting, diarrhea, fistulas, GI drainage, third spacing of fluids) have avid renal absorption of tubular sodium and urine sodium levels of less than 20 mEq/L, whereas those with hypovolemic hyponatremia due to renal causes (eg, diuretics, salt-losing nephropathy, aldosterone deficiency) have inappropriately elevated urine sodium levels in excess of 20 mEq/L.
Patients with hypervolemic hyponatremia due to decreases in effective circulating volume (eg, cirrhosis, nephrosis, congestive heart failure) have urine sodium levels of less than 20 mEq/L, whereas those with renal causes of hypervolemic hyponatremia or with SIADH have urine sodium levels in excess of 20 mEq/L.
Urine osmolarity may be helpful in establishing the diagnosis of SIADH.
Typically, patients with SIADH have inappropriately concentrated urine, with urine osmolarities in excess of 100 mOsm/L.
Patients with other forms of hyponatremia and appropriately depressed levels of ADH have urine osmolarities below 100 mOsm/L.
Serum thyroid-stimulating hormone (TSH) and free thyroxine levels should be checked if the clinical presentation is consistent with hypothyroidism.
Adrenal function should be assessed, via random serum cortisol levels or adrenocorticotropic hormone (ACTH) stimulation test, in patients who have recently taken oral steroids or in any patient suspected of having cortisol deficiency.
Imaging Studies
Imaging studies may be indicated depending on the underlying etiology of the hyponatremia (eg, chest radiograph in a patient with congestive heart failure).
Usually, a head CT scan is indicated in the patient with altered mental status to ensure that no other underlying cause for the mental status is present.

19. 2. What other laboratory tests are needed to be requested for the patient?
Serum glucose concentration
Several physiologic states (e.g. hyperglycemia) exist in which correct laboratory analysis yields low serum sodium levels, but these levels do not reflect a true hypoosmolar state.
Accumulation of extracellular glucose induces a shift of free water from the intracellular space to the extracellular space
Serum sodium concentration is diluted by a factor of 1.6 mEq/L for each 100 mg/dL increase above normal serum glucose concentration
Lab Studies
The diagnosis of hyponatremia depends entirely on the ability to properly obtain a sample of the patient's serum and to accurately measure its concentration of sodium.
When interpreting serum sodium levels, always consider the possibility of sampling error, especially when the reported value does not seem consistent with the history or physical findings.
Was the patient's blood sample properly labeled?
Was it obtained from a venous site proximal to an infusion of hypotonic saline or dextrose in water?
Is laboratory measurement or reporting in error?
If an error is suspected, a second sample should be submitted for testing before therapeutic measures are initiated.
In addition to sampling and analysis errors, several physiologic states exist in which correct laboratory analysis yields low serum sodium levels, but these levels do not reflect a true hypoosmolar state.
The most common example is serum hyperglycemia.
Accumulation of extracellular glucose induces a shift of free water from the intracellular space to the extracellular space.
Serum sodium concentration is diluted by a factor of 1.6 mEq/L for each 100 mg/dL increase above normal serum glucose concentration.
Systemic osmolarity is normal or even increased, not decreased, as in true (ie, hypoosmolar) hyponatremia.
This hypertonic hyponatremia has no physiologic significance, and serum sodium concentration corrects as normoglycemia is reestablished.
A similar phenomenon is observed in patients treated with glycerol or mannitol in an effort to control acute glaucoma or intracranial hypertension. This phenomenon is also seen in patients with advanced renal disease who receive radiocontrast agents for diagnostic testing.
Hyponatremia may be noted in patients whose serum contains unusually large quantities of protein or lipid.
In these patients, an expanded plasma protein or lipid fraction leads to a decrease in the plasma water fraction in which sodium is dissolved.
Laboratory techniques that measure absolute sodium content per unit of plasma water report low sodium levels despite the fact that the concentration of sodium in serum water remains within the normal range.
This phenomenon, known as pseudohyponatremia, occurs when flame emission spectrophotometry or indirect potentiometry is used to assay serum sodium levels rather than direct potentiometry techniques. This occurs in approximately 60% of US laboratories.
Serum osmolarity remains undisturbed, and attempts at correcting serum sodium level are not indicated.
Hyperlipidemia that is severe enough to produce pseudohyponatremia almost always is accompanied by a notably lipemic appearance of the serum sample.
Hyperproteinemia of sufficient magnitude to induce pseudohyponatremia commonly is due to coexisting multiple myeloma.
Serum osmolarity is helpful in establishing the diagnosis of true hypoosmolar hyponatremia. Serum osmolarity is abnormally low in patients with hypoosmolar hyponatremia, but it is normal in patients with pseudohyponatremia due to hyperlipidemia or hyperproteinemia and normal or elevated in patients with hypertonic hyponatremia due to serum hyperglycemia.
Urine sodium levels are helpful in distinguishing renal causes of hyponatremia from nonrenal causes.
Patients with hypovolemic hyponatremia due to nonrenal causes (eg, vomiting, diarrhea, fistulas, GI drainage, third spacing of fluids) have avid renal absorption of tubular sodium and urine sodium levels of less than 20 mEq/L, whereas those with hypovolemic hyponatremia due to renal causes (eg, diuretics, salt-losing nephropathy, aldosterone deficiency) have inappropriately elevated urine sodium levels in excess of 20 mEq/L.
Patients with hypervolemic hyponatremia due to decreases in effective circulating volume (eg, cirrhosis, nephrosis, congestive heart failure) have urine sodium levels of less than 20 mEq/L, whereas those with renal causes of hypervolemic hyponatremia or with SIADH have urine sodium levels in excess of 20 mEq/L.
Urine osmolarity may be helpful in establishing the diagnosis of SIADH.
Typically, patients with SIADH have inappropriately concentrated urine, with urine osmolarities in excess of 100 mOsm/L.
Patients with other forms of hyponatremia and appropriately depressed levels of ADH have urine osmolarities below 100 mOsm/L.
Serum thyroid-stimulating hormone (TSH) and free thyroxine levels should be checked if the clinical presentation is consistent with hypothyroidism.
Adrenal function should be assessed, via random serum cortisol levels or adrenocorticotropic hormone (ACTH) stimulation test, in patients who have recently taken oral steroids or in any patient suspected of having cortisol deficiency.
Imaging Studies
Imaging studies may be indicated depending on the underlying etiology of the hyponatremia (eg, chest radiograph in a patient with congestive heart failure).
Usually, a head CT scan is indicated in the patient with altered mental status to ensure that no other underlying cause for the mental status is present.

20. 3. How will you manage the patient’s hyponatremia?
GOALS:
To raise the plasma Na+ concentration y restricting water intake and promoting water loss
To correct underlying disorder
MANAGEMENT
Check vital signs every 2 hrs
Check for changes neurologic status – seizures
Treat with Isotonic Saline (0.9 NaCl – 154 meq/L)
Calculate sodium deficit

21. Calculation of sodium deficit:
Target Na: 125 – 135 mEq/L (average: 130 meq/L)
Na deficit = 0.6 x wt. in kg X (desired Na – actual Na)
= 0.6 x (50 kg) x (130 – 123)
= 210 mEq/L
Correction rate: <0.5 meq/L/hr
First 8 hrs – 50% of calculated Na
Next 16 hrs – other 50%
Risk of development of Osmotic demyelination syndrome in rapid correction of hyponatremia

22. 3. How will you manage the patient’s hyponatremia?
Do not give hypertonic saline
may result to overcorrection  Central Pontine Myelinosis
Do not give hypotonic fluids until serum Na is > 125 mg/L
Correct K+ deficit

24. RT, 60 y/o female CC: vomiting 1 week PTA --- fever dysuria frequency
self-medicated with Paracetamol & unrecalled antibiotics
2 days PTA --- headache, body malaise, nausea & vomiting
(-) epigastric pain, diarrhea

25. ROS: unremarkable
Personal History:
non-smoker, non-alcoholic beverage drinker
Past medical history:
known hypertensive for 10 years
Telmisartan 40 mg
Hydrochlorothiazide 12.5 mg tablet OD
discontinued amlodipine due to bipedal edema
Family History:
(+) hypertension – father & mother
(-) Diabetes mellitus
(-) Tuberculosis

26. Physical Exam Conscious, coherent, wheel-chair-borne Weight 50 kg
Vital signs
BP: 120/80 supine; 90/60 sitting
CR: 90/min supine; 105/min sitting
RR: 20/min
T: 37o C
Warm, dry skin, dry buccal mucosa, no active dermatoses
WHEELCHAIR BORNE- The clinical manifestations of hyponatremia are related
to osmotic water shift leading to increased ICF volume, specifically
brain cell swelling or cerebral edema. Therefore, the symptoms
are primarily neurologic, and their severity is dependent on the
rapidity of onset and absolute decrease in plasma Na
concentration. Patients may be asymptomatic or complain of
nausea and malaise. As the plasma Na concentration falls, the
symptoms progress to include headache, lethargy, confusion, and
obtundation. Stupor, seizures, and coma do not usually occur
unless the plasma Na concentration falls acutely
below 120 mmol/L or decreases rapidly.
Warm, Dry skin, Dry buccal mucosa
- consequence of nausea and vomiting
- severe or repetitive vomiting results in disturbances in
acid-base balance, dehydration and electrolyte depletion
- GI loss due to vomiting and diarrhea predisposes the patient
to hyponatremia since there is a corresponding sodium loss
associated with water loss (replaced by inappropriately
hypotonic fluids, such as tap water, half-normal saline, or
dextrose in water)

27. Physical Exam Pink, palpebral conjunctivae, anicteric sclera
Supple neck, JVP 3 cm at 30o angle
Symmetrical chest expansion, clear breath sounds
Adynamic precordium, AB 5th at LICS, MCL, no murmurs
Flabby abdomen, w/ normoactive bowel sounds, soft, non-tender
Extremities: (-) edema, pulses full and equal
Neurological exam: normal

28. Drugs Generic name Type of drug Indication Paracetamol NSAIDs
analgesic, antipyretic
Telmisartan
ARB
essential HPN
Hydrochloro-thiazide
Diuretic
HPN
Amlodipine
CCB
HPN & angina

29. Laboratory results: CBC
N.V.
Hemoglobin
0.132 g/dL
12 – 16 g/dL ↓
Hematocrit
0. 35
WBC
12.5 x 109/L
4.5 – 11 x 109/L ↑
Neutrophils
0.88
0.40 – 0.70
Lymphocytes
0.12
0.22 – 0.44
** Increased WBC with predominance of neutrophils indicate presence of bacterial infection

30. Laboratory results RESULTS N.V. FBS 98 mg/dL < 100 mg/dL N BUN
Serum creatinine
0.9 mg/dL
< 1.5 mg/dL ↑
Serum Na
123 mmol/L
136 – 145 mmol/L ↓
Serum K
3.7 mmol/L
mmol/L

31. Urinalysis Result Normal Appearance Yellow, slightly turbid ♥
Straw – dark yellow, clear – hazy pH
6.0
4.5 – 7.8
Specific gravity
1.020
Albumin
(-)
Sugar

32. Urinalysis Result Normal Hyaline casts 5/hpf ♥ 0-2/lpf Pus cells
Up to 5/hpf
RBC
2-5/hpf, non-dysmorphic
0-5/hpf
Epithelial cells
Few
Bacteria
Moderate ♥
(-)

33. Slightly turbid urine Cloudy urine may not be pathologic
Turbidity may be due to precipitation of crystals or non-pathologic amorphous salts
Materials that can cause turbidity:
Phosphate ▫ RBCs
Uric acid ▫ Ammonium urates
Leukocytes ▫ Bacterial growth
Mucus ▫ Blood clots
Contamination
Increased number of epithelial cells ♥

34. Hyaline Casts
Can indicate mild to severe renal disease when increased in numbers
proteinuria of renal (eg., glomerular disease)
extra-renal (eg., overflow proteinuria as in myeloma) origin.
Can be found in healthy individuals after heavy exercise ♥

35. Pyuria
Greater numbers of pus cells generally indicate the presence of an inflammatory process somewhere along the course of the urinary tract
Acute infection of kidney (pyelonephritis)
Cystitis (bladder)
Urethritis (urethra)
Pyuria often is caused by urinary tract infections, and often significant bacteria can be seen on sediment preps, indicating a need for bacterial culture. ♥

36. Bacteruria Can be contamination from external sources
Rapidly multiply in improper stored specimen
With increased WBCs, indicative of urinary tract infection ♥