Far Eastern University – Nicanor Reyes Medical Foundation HYPOVOLEMIC HYPONATREMIA

IM 3B: NEPHRO – SODIUM DISORDERS - Cause: Decreased total body water and sodium
Dr. Arenas - A decrease in fluid volume will stimulate the release of your
ADH. Both here are decreased, but remember that the
TOTAL BODY WATER decrease of body water is lesser compared to sodium.
- ICF 55 – 75%
o K, organic phosphate esters Urine Na (done to determine if it is a renal cause)
- ECF 25 – 45% - Non renal loss < 20 meq/L
o Intravascular (plasma) to extravascular (interstitial) o Good response to IV normal saline
space ratio 1:3 o Kidneys are responding appropriately
o Starling forces o Diarrhea as the most common cause
o Na, Cl, HCO3 - Renal loss > 20 mEq/L
o May be due to diuretic excess
OSMOLALITY - With signs of hypovolemia
- Solute / particle concentration of fluid (mOsm/kg) o Hypovolemia stimulates release of AVP increased
water reabsorption
o Gold standard for diagnosis: correction of serum Na
after hydration with normal saline.
o Only one that will be improved by normal saline
- 280 – 295 mOsm / kg
- ICF osmolality = ECF osmolality HYPERVOLEMIC HYPONATREMIA
- Primary determinant: sodium - Cause: Increase total body NaCl with greater increase in
- Key effectors: total body water.
o Water intake (thirst) – will be stimulated during - The retention of total body water is greater than that of the
hyperosmolar state sodium.
o Vasopressin (AVP) secretion (aka antidiuretic - Seen among Na-avid edematous disorders (CHF, cirrhosis,
hormone) – reabsorbption of water in hyperosmolar nephrotic syndrome)
state - Urine Na of hypovolemic hyponatremia to determine
o Renal water transport whether no renal or renal loss.

SODIUM DISORDERS EUVOLEMIC HYPONATREMIA

- Subclinically volume-expanded (NO edema)
HYPEROSMOLAR DISORDERS HYPOOSMOLAR DISORDERS
- SIADH as the most frequent cause
- Hypernatremia - Hyponatremia o Pulmonary disease, CNS disease
- Plasma Na >145 - Plasma Na <135 o Small cell lung carcinoma
o Selective serotonin uptake inhibitors
- Deficiency of body water - Excess of body water
relative to body solute relative to body solute
- Caused by abnormalities in water homeostasis

HYPONATREMIA
- Plasma Na < 135 mM and should have a low osmolality
- Occurs in 21% of hospitalized patients
- Causes:
o Increased circulating AVP
o Increased renal sensitivity to AVP
o Free water intake
- Acute: < 48 hrs
- Chronic: >48 hrs

FALSE / PSEUDOHYPONATREMIA
- Hyponatremia with normal or increased plasma osmolality
- Cause: hyperlipidemia, hyperproteinuria

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 HYPONATREMIA AND LOW SOLUTE INTAKE o F>M
- Inadequate dietary intake of solutes (rare cause of hyponat) o Early symptoms: N / V, headache
- Beer proteinuria o Severe symptoms: seizure, brainstem herniation,
o When patients takes in more beer but have less of the coma, death
solutes. o Key complication: normocephalic / hypercapneic
o Beer has a low Na and CHON content respiratory failure
- Hypovolemic due to dehydration o Usually iatrogenic (due to giving hypotonic fluids ---
- Low urine osmolality <100-200 mOsm/kg lycine – increases natriuresis ; diarrheal induced pre
- Urine Na < 10 - 20 mM op medications / preparations; thiazides also
increases natriuresis)
HYPOVOLEMIC EUVOLEMIC HYPERVOLEMIC
increase in total-
body Na+-Cl–
that is
accompanied by
Neurohormonal a
Underlying
MECHANISM activation, proportionately
cause
Increase in AVP greater increase
in total-body
water, leading to
a reduced
plasma Na - Chronic hyponatremia
GI loss (e.g., o Less likely to have severe symptoms because the brain
vomiting, has already adapted to the change of osmolality
diarrhea, tube o Subtle gait and cognitive defects, vomiting, nausea,
drainage) and confusion, seizure (Na < 125 mM)
insensible loss o Increased risk of falls seen in elderly
(sweating, o May even be asymptomatic
burns) Sodium-avid
reflux edematous DIAGNOSTIC EVALUATION
nephropathy, Hypothyroidism disorders - Determine volume status
interstitial Glucocorticoid (congestive - Determine possible cause: drug history, nausea, pain
DISEASES
nephropathies, deficiency heart failure o Nausea can cause vasopressin secretion
postobstructive SIADH [CHF], cirrhosis, - Radiologic imaging
uropathy, and nephrotic - Serologic osmolality
medullary cystic syndrome o Exclude pseudohyponatremia
disease, and - BUN, Creatinine, K
the recovery o K for aldosteronism checking
phase of acute - Serum glucose
tubular necrosis. o Decrease plasma Na by 1.6 – 2.4 mM for every 100
Thiazide mg/dL increase in serum glucose
diuretics o Hyperglycemia = hyponatremia
Urine Na+ - Serum uric acid (to determine whether SIADH and
<20 mM-Non Hypovolemic patient)
>30 mM : concentration is
URINE NA renal o Low UA / <4 UA – SIADH
SIADH typically very
>20 mM-Renal o High UA / >4 - Hypovolemic patient
low, <10 mM,
- Urine electrolytes
CLINICAL FEATURES o Urine Na : renal vs non renal loss
- Neurologic (predominant) § To determine whether patient is responding
- Cerebral edema (cellular swelling) increases ICP to treatment
- Acute symptomatic hyponatremia o Urine K : calculate urine-to-plasma electrolyte ratio
o Medical emergency (predicts response to fluid restriction)

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 - Urine osmolality ACUTE SYMPTOMATIC HYPONATREMIA
o < 100 mOsm / kg : Polydipsia - Hypertonic 3% saline (513 mM)
o > 400 mOsm / kg : Vasopresin excess o Goal: increase plasma Na by 1-2 mM/h (total 4- 6
o Intermediate multifactorial mM/h)
o After achieving the desired goal, the next step is to
TREATMENT alleviate severe acute symptoms by following the
- Withdrawal of underlying cause corrective guidelines for chronic hyponatremia (see
- Consideration above)
o Presence / severity of symptoms - Na deficit = 0.5 x body weight x (target plasma Na –
o Duration: acute vs chronic starting plasma Na)
§ Chronic risk for Osmotic Demyelination o Always remember, the target plasma Na may not be
Syndrome (ODS) if plasma Na is corrected by the normal Na level, especially if the severely low.
>> 8 – 10 mM within 24 hrs or > 18 mM within o Remember that your target is at a maximum of 10 in
48 hours 24 hrs.
§ So this is why during chronic cases, we treat o So if you have a serum Na of 110, your target will be
the patient very slowly. Rapid correction may 120 in a day, not the lower limit of the normal. You
lead to ODS. will achieve the normal in succeeding days.
§ target change in 24 hours is a maximum of 10 o Mag aadd add naman yan e. Gets?
mM and a maximum of 18 within 48 hours - Monitor plasma Na every 2 – 4 hours
§ at risk for ODS: alcoholics and hypokalemic
patients CHRONIC HYPONATREMIA
o What happens in ODS? - Prevent ODS (increased risk: alcoholism, hypokalemia)
§ In hyponatremia, the cells will push out - Increase plasma Na:
osmoles to reach an equilibrium which is the o < 8 – 10 mM in 24 hours
way the brain adapts. Adaptation usually o < 18 mM in 48 hours
occurs in 48 hours. - Water deprivation (cornerstone of treatment)
§ If very rapid correction, the extracellular - urine – to – plasma electrolyte ratio = urine Na + K /
osmoles will draw water from the cells causing plasma Na
the cells of the brain to shrink which is the root o ratio > 1 : < 500 mL/day
cause of the symptoms felt in ODS o ratio 1 : 500 – 700 mL/day
o Response to intervention is unpredictable o ratio < 1 : < 1 L/day

SIADH
- Furosemide 20 mg 2x a day (to increase free water loss) +
oral salt tablet (to prevent further hyponatremia)
- Demeclocycline (only give this if other treatment fails)

HYPOVOLEMIC HYPONATREMIA
- Isotonic normal saline

EUVOLEMIC HYPONATREMIA
- Treat underlying cause
- Give AVP antagonists:
o Approved for the management of all but hypovolemic
hyponatremia and acute hyponatremia
§ SIADH, hypervolemic hyponatremia
o Tolvaptan: oral V2 antagonist
This is called Osmotic Demyelination Syndrome (ODS). The symptoms include dysarthria, o Conivaptan: Intravenous V1, V2 antagonist
dysphagia, paraparesis, behavioral disturbances, lethargy, confusion, disorientation,
obtundation, and coma, which are often irreversible or only partially reversible. Severely
affected patients may become “locked in”; they are awake, but are unable to move HYPERVOLEMIC HYPONATREMIA
or communicate.These symptoms typically delayed for two to six days after overly rapid
correction of Na. - Treat CHF, cirrhosis, nephrotic syndrome.
- Give AVP antagonist
o Tolvaptan: oral V2 antagonist

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 o Conivaptan: Intravenous V1, V2 antagonist CENTRAL DI
- NOTE: Do not give AVP antagonist among SIADH and - Inadequate secretion and deficient synthesis of AVP in the
hypovolemic patients, for it will further aggravate the state hypothalamic neurohypophyseal system
of hypovolemia. - Will respond to DDAVP

HYPERNATREMIA NEPHROGENIC DIABETES CENTRAL DI

- Plasma Na > 145 mM INSIPIDUS
- Result of combined water and electrolyte deficit: Renal resistance to AVP Inadequate secretion and
o water loss > Na loss deficient synthesis of AVP
- Ingestion / iatrogenic: less frequent cause Not respond to DDAVP Will respond to DDAVP
- Elderly: highest risk
o Mainly because they have a decrease threshold for GESTATIONAL DI
thirst - Increase levels of vasopressinase
o This will metabolize oxytocin which will prevent
NON RENAL premature contractions. However, it also metabolizes
- Insensible losses: increased in fever, exercise, heat the vasopressin and enhances its excretion.
exposure, burns - Will also respond to DDAVP
- 10 ml/kg/day (eg 700 mL in a 70 kg person)
- Diarrhea : most common GI cause CLINICAL FEATURES
o Osmotic diarrhea and viral gastroenteritis - Neurologic
RENAL o Cellular shrinkage
- Osmotic diuresis: o Altered mental status: most frequent manifestation
o Happens when there is non reabsorbable solutes in o Acute hypernatremia
your tubules causing impairment of water § Parenchymal / subarachnoid hemorrhage,
reabsorption. Water will remain in the tubules à will subdural hematoma / Stroke
secrete water § More common in pediatric / neonatal patients
o Increase in urinary solute excretion and urine o Rhabdomyolysis
osmolality - Chronic hypernatremia
o Seen in: o Less severe symptoms
§ Hyperglycemia
§ Excess urea DIAGNOSIS
§ Post obstructive diuresis - HISTORY
§ Mannitol o Presence / absence of thirst Polyuria
- Water diuresis: o Extrarenal source of water loss (eg diarrhea)
o Due to insufficient vasopressin - Physical Examination
o Diabetes insipidus (central / nephrogenic) clinical o Assessment of ECF status
syndrome characterized by excretion of abnormally o Detailed neurologic exam
large volume of urine (diabetes) that is dilute - Accurate monitoring of daily fluid intake and urine output.
(hypotonic) and devoid of taste from dissolved solutes
o In DM, hypertonic and sweet tasting DIAGNOSIS
- Serum osmolality: > 295 mOsm/kg
NEPHROGENIC DIABETES INSIPIDUS - Urine osmolality: concentrated urine (Eg >500 mOsm/kg)
- Renal resistance to AVP (normal levels of AVP; kidneys not
utilizing this properly)
- Genetic
- Acquired
o Hypercalcemia, hypokalemia
o Lithium, ifosfamide
- Will fail to respond to Desmopressin (DDAVP)

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 FREE WATER DEFICIT
- [ (Na – 140) / 140 ] x TBW
o TBW = 50% of body weight for females and 60% in
males
o Administer over 48 – 72 hours
o Avoid correction of plasma Na by > 10mM / day
o Example: 70 kg, female, serum Na 155
§ TBW: 70 X 0.6 = 35
§ Water deficit = [ 155 – 140 / 140 ] x 35
§ Water deficit = 3.75 L

CENTRAL DI
- IV / intranasal / oral DDAVP
- So just replace the Vasopressin

NEPHROGENIC DI
- Thiazides, NSAIDs
- If secondary to Lithium intake:
o Amiloride 2.5 – 10 mg/day
o Increase water intake

TREATMENT
- Correct / withhold underlying cause
o Drugs
o Hyperglycemia
o Hypercalcemia
o Hypokalemia
o Diarrhea

- Administer free water (electrolyte free water)

o Per orem or by NGT
o IV: D5W, hypotonic saline (1/4 or ½ normal saline)

Notes from Lecture PPT, Leslee Cruz Trans

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