hypernatremia. serum na concentration > 145 meq/l deficit of total body water relative to total...
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Hypernatremia
• serum Na concentration > 145 mEq/L• deficit of total body water relative to total
body Na
http://www.merck.com/mmpe/sec12/ch156/ch156e.html#CIHJIJEB
Causes of hypernatremia
Description Category Examples
Hypovolemic hypernatremia
Decreased TBW and Na with a relatively greater decrease in TBW
GI losses DiarrheaVomiting
Skin losses BurnsExcessive sweating
Renal losses Intrinsic renal diseaseLoop diureticsOsmotic diuresis (glucose, urea, mannitol
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Hypovolemic hypernatremia
• Na loss accompanied by a relatively greater loss of water from the body
• Loop diuretics inhibit Na reabsorption• most common cause of hypernatremia due to
osmotic diuresis is hyperglycemia in patients with diabetes
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Causes of hypernatremiaDescription Category ExampleEuvolemic hypernatremia
Decreased TBW with near-normal total body Na
Extrarenal losses from respiratory tract
Tachypnea
Extrarenal losses from skin Excessive sweatingFever
Renal losses Central diabetes insipidusNephrogenic diabetes insipidus
Other Inability to access waterPrimary hypodipsiaReset osmostat
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Euvolemic hypernatremia
• decrease in TBW with near-normal total body Na (pure water deficit)
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Causes of hypernatremiaDescription Category Examples
Hypervolemic hypernatremia
Increased Na with normal or increased TBW
Hypertonic fluid administration
Hypertonic salineNaHCO3 TPN
Mineralocorticoid excess Adrenal tumors secreting deoxycorticosteroneCongenital adrenal hyperplasia (caused by 11-hydroxylase defect)
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Hypervolemic hypernatremia
• grossly elevated Na intake associated with limited access to water
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Causes of hypernatremia• Net water loss
– Pure water– Unreplaced insensible losses (dermal and respiratory)– Hypodipsia– Neurogenic diabetes insipidus– Post-traumatic– Caused by tumors, cysts, histiocytosis, tuberculosis,– sarcoidosis– Idiopathic– Caused by aneurysms, meningitis, encephalitis,– Guillain–Barré syndrome– Caused by ethanol ingestion (transient)– Congenital nephrogenic diabetes insipidus– Acquired nephrogenic diabetes insipidus– Caused by renal disease (e.g., medullary cystic disease)– Caused by hypercalcemia or hypokalemia– Caused by drugs (lithium, demeclocycline, foscarnet,– methoxyflurane, amphotericin B, vasopressin V– receptor antagonists)
Adrogue, H., and N. Madias. Hypernatremia.The New England Journal of Medicine. Volume 342 Number 20.
Causes of hypernatremia• Hypotonic fluid
– Renal causes– Loop diuretics– Osmotic diuresis (glucose, urea, mannitol)– Postobstructive diuresis– Polyuric phase of acute tubular necrosis– Intrinsic renal disease– Gastrointestinal causes– Vomiting– Nasogastric drainage– Enterocutaneous fistula– Diarrhea– Use of osmotic cathartic agents (e.g., lactulose)– Cutaneous causes– Burns– Excessive sweating
Adrogue, H., and N. Madias. Hypernatremia.The New England Journal of Medicine. Volume 342 Number 20.
Causes of hypernatremia• Hypertonic sodium gain
– Hypertonic sodium bicarbonate infusion– Hypertonic feeding preparation– Ingestion of sodium chloride– Ingestion of sea water– Sodium chloride–rich emetics– Hypertonic saline enemas– Intrauterine injection of hypertonic saline– Hypertonic sodium chloride infusion– Hypertonic dialysis– Primary hyperaldosteronism– Cushing’s syndrome
Adrogue, H., and N. Madias. Hypernatremia.The New England Journal of Medicine. Volume 342 Number 20.
Clinical Features of Hypernatremia• altered mental status• weakness• neuromuscular irritability• Focal neurologic deficits• Occasionally, coma and seizures• Polyuria• thirst• Increased risk of subarachnoid or intracerebral hemorrhage
due to decreased brain cell volume• Signs and symptoms of volume depletion often present in
patients with history of excessive sweating, diarrhea, or an osmotic diuresis
DIAGNOSIS
• can be induced by the administration of sodium in excess of water
• a high plasma sodium concentration most often results from free water loss
• appropriate renal response is excretion of the minimum volume (500 mL/d) of maximally concentrated urine (urine osmolality 800 mosmil/kg)
• can be induced by the lack of replacement
• or by urinary losses due to central or nephrogenic diabetes insipidus or to an osmotic diuresis resulting from increased excretion of glucose in uncontrolled diabetes mellitus or of urea with high-protein feedings
• CDI and NDI can generally be distinguished by administering desmopressin (10 ug intranasally) after careful water restriction
• Urine osmolality should increase by at least 50% in CDI
Hypernatremia
Treatment
Treatment Goals
• To determine the rate of correction• To correct the water deficit and hypovolemia
at the rate desired• To correct the underlying disorder, thereby
reducing ongoing water loss
Rate of correction
• Depends on the acuity of its development and the presence of neurologic dysfunction
1. Symptomatic hypernatremia– Aggressive correction -> potentially dangerous – Rapid shift of water into brain cells -> increase risk
of seizures and permanent neurologic damage– Water deficit: reduced gradually: 10 to 12
mEq/L/d
Rate of correction
2. Chronic asymptomatic hypernatremia– Cerebral adaptation to the chronic hyperosmolar
state -> increased risk of treatment-related complication
– Plasma Na+ : lowered at a more moderate rate• Between 5 and 8 meq/L/d
Fluid administration
• Mainstay: administration of water– Preferably be mouth or NGT
• Alternative: D5W or quarter normal saline IV– D5W: pure water loss as in insensible losses or
diabetes insipidus– Quarter normal saline: concurrent electrolyte loss
as in GI and diuretic-induced losses
Fluid administration
• Traditionally..– Free water deficit= {([Na] – 140)/140} x (TBW)
• Does not provide sufficient guidance regarding the rate and the content of the infusate
Fluid administration
• Estimated change in [Na+] from fluid administration:∆ [Na+] = {[Na+
i] + [K+i] - [Na+
s]} ÷ {TBW + 1}
– [Na+i] and [K+
i]: concentration in infused fluid
– [Na+s]: starting serum sodium
– Estimated TBW:• Men: Lean Weight (kg) x 0.5• Women: Lean Weight (kg) x 0.4
Water deficit
• Water deficit: corrected slowly over at least 48–72 h
• To calculate the rate of water replacement:– Check for ongoing losses– plasma Na+ concentration should be lowered by
0.5 mmol/L per h– not more than 12 mmol/L over the first 24 h
50 kg female: [(132-140)/140] x (0.4 x 50kg) = 1.14 L free-water deficit
For example …A 70kg with diarrhea (2L/d) from laxative abuse presents
with obtundation and [Na+] = 164meq/L, [K+] = 3.0. A replacement fluid of D5W with 20mEq KCl/L is chosen.
• The ∆ [Na+] with 1 L of this fluid would be -4mEq/L.– {0 + 20 - 162} ÷ {(70x0.5) + 1} = - 4mEq/L
• 3L is necessary for a ∆ [Na+] - 12 mEq/L/24hr– (-12mEq/L/d) ÷ (- 4mEq/L/L of solution)
• Hourly rate of infusion: 125cc/hr (3L/d ÷ 24hr/d)• Close follow-up as it does not account for ongoing GI
or insensible losses, which may account for another 1.4L/d of water required to keep [Na+] stable.
Specific therapies for underlying cause
• Hypovolemic hypernatremia– Mild volume depletion: 0.45% NS used to
replenish EDF and water deficit– Severe volume depletion: isotonic fluid over
correction of the hyperosmolar state• Once stable: give hypotonic fluid to replace the free
water deficit
Specific therapies for underlying cause
• Hypernatremia from primary Na+ gain– Cessation of iatrogenic Na
• Diabetes insipidus:– Treatment directed toward symptomatic polyuria– Central DI: impaired secretion of vasopressin
• Tx: administration of dDAVP (vasopressin analog)– Nephrogenic DI:
• Tx: low Na+ diet combined with thiazide diuretics -> enhances proximal reabsorption of salt and water - > decrease excess water loss
• Decrease protein intake -> minimize solute load excreted -> decrease urine output
Specific therapies for underlying cause
• Partial Central Diabetes Insipidus• chlorpropamide, clofibrate, carbamazepine,
NSAIDs• stimulate AVP secretion or enhance its action
on the kidney
Specific therapies for underlying cause
• Nephrogenic Diabetes Insipidus• Treat underlying cause, eliminate offending drug• Symptomatic polyuria: low-Na+ diet and thiazide diuretics
– induces mild volume depletion, → enhanced proximal reabsorption of salt and water, decreased delivery to the collecting duct (site of action of AVP)
• NSAIDs: potentiate AVP action → increase urine osmolality, decrease urine volume
• Amiloride: on lithium– nephrotoxicity of lithium requires the drug to be taken up into
collecting duct cells via the amiloride-sensitive Na+ channel