a new perspective on hypernatremia
TRANSCRIPT
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A New Perspective on Hypernatremia
Taipei Veterans General Hospital, Hsin-Chu branch
Director of Nephrology
Steve Chen
Na
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SodiumSodium
Reference Range:136 – 145 meq/L
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SodiumSodium
Hypernatremia is Na+ > 150 meq/L
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Pathophysiology(1)Pathophysiology(1)
– Primary MechanismsPrimary Mechanisms Renal response to ADHRenal response to ADH
– Conservation of free waterConservation of free water– ↓↓ Urine output with osmolality > 1000 mosm/kgUrine output with osmolality > 1000 mosm/kg
Failure of ADH responseFailure of ADH response– Inability to excrete NaInability to excrete Na++ properly properly– Urine osmolality 200-300 mosm/kgUrine osmolality 200-300 mosm/kg– Urinary NaUrinary Na++ 60-100 meq/kg 60-100 meq/kg
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Pathophysiology(2)Pathophysiology(2)
– Rapid hypertonicity Rapid hypertonicity Loss of 10% of body weight Loss of 10% of body weight
– “ “Doughy” skin turgorDoughy” skin turgor CNS cellular dehydrationCNS cellular dehydration
– Hemorrhage: ICH/SAHHemorrhage: ICH/SAH– Tearing of cerebral blood vessels, then 2° brain Tearing of cerebral blood vessels, then 2° brain
shrinkageshrinkage– Gradual hypertonicityGradual hypertonicity
Idiogenic osmoles prevent brain shrinkageIdiogenic osmoles prevent brain shrinkage
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Etiology of Etiology of HypernatremiaHypernatremia
Etiology(1)Etiology(1)– Excessive sodium intakeExcessive sodium intake
Iatrogenic NaIatrogenic Na++ administration administration Sea water ingestionSea water ingestion Mineralocorticoid or glucocorticoid excessMineralocorticoid or glucocorticoid excess
– Pure water lossPure water loss Inability to swallow, bedridden, comatoseInability to swallow, bedridden, comatose
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Etiology of Etiology of Hypernatremia Hypernatremia
Etiology(2)Etiology(2)– Loss of waterLoss of water
RenalRenal– Central Diabetes InsipidusCentral Diabetes Insipidus– Impaired renal concentrating abilityImpaired renal concentrating ability
DrugsDrugs– Alcohol, Lithium, Phenytoin, Propoxyphene, Alcohol, Lithium, Phenytoin, Propoxyphene,
SulfonylureasSulfonylureas
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Etiology of Etiology of Hypernatremia Hypernatremia
Etiology (3)Etiology (3)– Loss of water > NaLoss of water > Na++
Skin loss: Burns, sweatingSkin loss: Burns, sweating Peritoneal dialysisPeritoneal dialysis GI loss: Vomiting, diarrhea GI loss: Vomiting, diarrhea
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Symptoms & Signs Symptoms & Signs
Clinical Features: mainly CNSClinical Features: mainly CNS– Acute symptoms at Acute symptoms at NaNa++ > 158 meq/L > 158 meq/L
OsmolOsmol– Restless, irritabilityRestless, irritability 350-375350-375– Tremulousness, ataxiaTremulousness, ataxia 375-400375-400– Hyperreflexia, twitching, spasticityHyperreflexia, twitching, spasticity
400-430400-430– Seizures and deathSeizures and death > 430> 430
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TypesTypes of Hypernatremia of HypernatremiaHypernatremia with low body sodium
content
Hypernatremia with normal body sodium content
Hypernatremia and increased body sodium content
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Hypernatremia with Hypernatremia with lowlow total total body sodium contentbody sodium content
Water loss in excess of sodium loss
Osmotic diuresis Diarrhea Sweating Vomiting
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Hypernatremia with Hypernatremia with normalnormal total total body sodium contentbody sodium content
Due to water loss
Diabetes insipidus Central diabetes insipidus Nephrogenic diabetes
insipidus
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Hypernatremia and Hypernatremia and increasedincreased total body sodium contenttotal body sodium content
Following administration of large quantities of hypertonic saline solutions
Iatrogenic Na administration: FFP… Sea water intake Mineralocorticoid or glucocorticoid
excess
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Flow chart of DDFlow chart of DD ECF volume Increased Hypertonic Na
Not increased
Minimun volume of maximum concentrated urine
Yes
Extra-renal Insensible water loss GI
No Urine osmole excretion rate > 750 mosmol/day
Osmotic diureticDiuretics
YesNo
Renal response to DDAVP Urine osmolality↑
CDIYes
No
NDI
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Hypernatremia Hypernatremia Q1: What is the ECF volume?
A gain of Na is rarely the sole cause of hypernnatremia
Q2: Has the body weight changed? Water shift with convulsion or rhabdomyolysis rarely : 10-15meq/L
Q3: Is the thirst response to hypernatremia normal? ↑1% Na is powerful urge to drink ﹝ ﹞
Q4: Is the renal response to hypernatremia normal? Urine osmolarity > 1000mOsm/KgH2O Urine volume=20mL/H unless there is a high rate of excretion of effective osmoles
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Goals of therapyGoals of therapy
To correct water deficit
To stop ongoing water loss
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Principles of therapyPrinciples of therapyCorrection should be done over
48 to 72 hours
Hypotonic solution like 5% dextrose
Plasma Na should be lowered by 0.5 meq/L/hr or not more than 12meq/L/ 24 hrs
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Total Water Deficit = A+B+CTotal Water Deficit = A+B+CIf it results only from water loss, then Current
total body osmoles = Normal total body osmoles CBWa x plasma Na = NBWa x 140 ﹝ ﹞Water deficit (A)
= NBWa - CBW a = CBWa x
plasma Na /140- 1﹛ ﹝ ﹞ ﹜ Estimated insensible loss (B) = 30-50ml/HRenal water loss, ongoing (C)
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Guidelines of therapyAdministration of IV Fluids
– (Isotonic Salt ~ Free)Encourage foods: low in Na+
Push P.O. FluidsMonitor Neurological statusMonitor for Arrhythmias
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PolyuriaPolyuria
Polyuria based on an unexpectedly low urine osmolality (UO)
If renal medulla is damaged, UO is close to that of plasma when ADH acts( 300mOsm/Kg)
If ADH fails, UO is below 300 mOsm/Kg
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Urine Specific GravityUrine Specific Gravity
USG defined as weight of solution compared with that of an equal volume of distilled water
USG ∞ particle weight X particle number Urine osmolality ∞ particle number
Normally(neither glucose nor protein in urine), ↑SG 0.001=↑UO 30-35mosmol/Kg SG (1.010) = UO( 300-350)
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Polyuria Polyuria
Polyuria as a function of osmole excretion rate= urine osmolality x urine volume (UV)
Normally, osmole excretion rate = 900mOsm/D if urine osmolality is 900, UV is 1 L
In osmotic diuresis, osmole excretion rate =1800mOsm/D , which is exogenous(Glucose) if urine osmolality is 900, UV is 2L in fact, urine osmolality is 450, UV is 4L
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Polyuria Polyuria Appropriate Inappropriate
Water diuresis(Uosm<250mosmol/Kg)
IV dilutionPrimary hypodipsia
CDINDI
Solute diuresis(Uosm>300mosmol/Kg)
Saline loadingPost-obstructive
HyperglycemiaHigh-protein tube feedingNa-wasting nephropathy
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Urine osmolatity (mosmol/Kg)
Clinical settings Response to ADH
<300 CDINDI
+--
300 to 800 Osmotic diuresisCDI, partialNDI, partialVolume depletion in CDI
--+--+
>800 Non-renal water loss primary hypodipsia Na overload
----
Variable Essential hypernatremia
Variable
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Renal water loss in NDIRenal water loss in NDILithium-induced NDI with hypernatremia
150ml/H of isosmotic urine(=325mosmol/Kg)Urine urea/amonium is ineffective particle
Urine Na+K con. affect plasma Na con. ﹙ ﹚Urine Na+K =60meq/L﹙ ﹚ ;
Plasma Na+K =150meq/L ﹙ ﹚ Effective urine osmolarity=40% that of plasma
Renal water loss= 150ml/H x 60%
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Hypernatremia-Na gainHypernatremia-Na gain
Half normal saline in lithium-induced NDI Normal saline in glucose-induced osmotic diuresis
Hypertonic NaHCO3 in cardiac arrest Dialysis error( hypertonic dialysate) Salt poisoning in infants Ingestion of sea water FFP plus Lasix in burned patients Combination of above and thirst center defect
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Reset HyponatremiaReset Hyponatremia Normal osmoreceptor response to change in
plasma osmolarity: plasma Na 125﹝ ﹞ ~ 130meq/L
Clinical settings: Hypovolemic states: baroreceptor stimulus Quadriplegia: ↓ effective volume Psychosis Defective cellular metabolism: TB meningitis Pregnancy: hCG
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Reset Hypernatremia Reset Hypernatremia Inhibition of ADH release and excretion of a dilute
urine after water loading Stimulation of ADH release and excretion of a
concentrated urine after water deprivation Maintenance of new normal plasma Na within ﹝ ﹞
narrow limits(±1-2%): 140±2.8meq/L( 137 ~ 143) Clinical setting: Primary hyper-aldosteronism reset
Na > 145meq/L﹝ ﹞ , restored by hormone manipulation or lowering the effective volume with diuretic
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Essential hypernatremiaEssential hypernatremiaPrimary hypo-dipsia (thirst center defect)
plus inhibition of ADH (osmoreceptor defect) New normal plasma Na : wide variation ﹝ ﹞
between 150 and 180meq/LOsmoreceptor relatively insensitive
rather than being reset at a higher level; selectively damaged ; normal response to volume
Chlorpropamide: ↑ ADH effect
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SIADH: drug related SIADH: drug related ADH ↑ ADH ↑ADH preparations:
DAVdP(Desmopressin), Aqueous vasopressin, Lysine-vasopressin in nasal spray, Vasopressin tannate in oil
Potentiate ADH effect Chlopropamide, Cabamazepine, NSAIDs
Increase ADH secretion Clofibrate
Drug not requiring ADH Thiazide ± Amiloride
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