hyponatremia by akram
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Hyponatremia Management
Dr. Fateh AkramDTCD STUDENTMedicine Unit VI
National Institute of Diseases of The Chest & Hospital
Normal water balanceNormal water intake(1-1.5 L/d)
Intracellular ExtracellularCompartment compartment28 L 14 L
42 L TBW60% of body weight
Fixed water excretionStool Sweat Lungs0.1 L/d 0.1 L/d 0.3 L/d
Total insensible losses0.5 L/d
WaterOfCellularMetabol0.3-0.5 L/d
Variable water excretion
Kidney
Total urine output1-1.5 L/d
Waterintake
Waterexcretion
ADH
Hyponatremia Supervenes when
free water intake >> free water excretion
Main defense excretion of free water by kidneys
Hypotonic HyponatremiaHypovolemic Euvolemic Hypervolemic
Urine Na
<30 >30ExtraRenal Renal
1.Diarrhea2.Vomiting3.Hemorrhage4.Sweating
1.Diuretics2.Mineralocorticoid def3.Salt losing Nephropathies4.Cerebral salt wasting
1.SIADH 2.Glucocorticoid def3.Hypothyroidism4.Poor solute intake -Tea Toast syndrome - Beer potomania5.Post op / Hospital acquired
1.CHF2.Cirrhosis3.Nephrotic synd4.Advanced CRF
Hypotonic hyponatremia(Vol status indeterminate)
Urine Na <30 : Respond to 0.9 NS Volume depleted
Urine Na > 30 : No response to 0.9 NS Likely to have SIADH
SIADH
Criteria for diagnosis:
P osm <275 mOsm/kg U osm >100 mOsm/kg Clinical euvolemia Urine Na > 30mmol/L while on normal salt intake Normal thyroid, adrenal and renal functions Inappropriately elevated AVP levels in 85-90%
Tumors small cell CA, Head & NeckCNS Trauma, tumors, meningitis, CVAPulmonary Pneumonia, PTB, resp failure, asthma
Mechanical ventilation, COPDDrugs DDAVP, Diabinese, NSAIDS, opiates,
Carbamazepine, SSRI, Tricyclic, ThiazidesEcstasy, ACE-I, Omeprazole
Miscellaneous Pain, Nausea, surgery, stress, Alcohol withdrawal
SIADH : Common Causes
SIADH : Treatment
Discontinue offending agent Treatment of etiology (infection, pain) Fluid restriction (for Chronic asymptomatic
Hyponatremia)
Euvolemic Hypotonic hyponatremiaPoor solute Intake
Beer Potomania, Tea Toast syndrome
Urine Volume =
Normal Urinary Electrolytes Normal Urinary Urea
Na+ , K+ = 150 + 50 = 200 Catabolism= 75-100
Accompanying anions= 200 Diet ~50 mM/10 gm of dietary protein
Total 400 mM/day Total 400-500 mM/day
Urinary solute excretionUrinary Osmolality
Clinical setting of low solute intake: - Alcoholism (Beer Potomania) - Anorexia (Tea and Toast Diet)
Urinary solute excretion in person on normal diet-800-900 mM/day
Euvolemic Hypotonic hyponatremiaPoor solute Intake
Treatment
1. Increase solute intake –• High protein diet• Salt tablets or high dietary
salt• Urea
2. Fluid restriction
Hospital acquired HyponatremiaVirtually every hospitalized patient has
potential stimulus for AVP excess Administration of hypotonic fluid with
excess AVP are at risk for Hyponatremia
Chung HM et al, Arch Inter Med 2002
Hospital acquired hyponatremia• Ringer’s Lactate (Sodium 77) is hypotonic
and can produce hyponatremia• No justification for Ringers lactate in post op
period• Administration of 0.9 saline is safe• No reports of 0.9 Saline causing neurological
complications of hyponatremiaSteele A et al, Ann Intern Med 1997Moritz ML et al, J Am Soc Nephrol 2005
Cerebral adaption to decrease cerebral edema
Early 1-3 hrsCSF distribution
Later (> 3 hrs)Loss of Osmolytes and electrolytes:
Glutamate, Inositol, Taurine, Urea, K, Na, Creatinine
InvestigationHistory & volume statusSerum OsmolalityUrine Osmolality/sp grUrine NaS Cr/urea/KT3/T4/TSHCXRCT Scan Manisha Sahay
Extensive data suggest that the serum sodium should be raised by no more than 10 mEq/L over 24 hours. Correction by 6 mEq/L in 24 hours has been dubbed the "rule of sixes."The rule of sixes is as follows: "Six-a-day makes sense for safety. Six in 6 hours for severe symptoms and stop."
Acute Hyponatremia: Less than 48 hrs Neurologic symptoms due to brain edema Rapid correction well tolerated
Chronic Hyponatremia:More than 48 hrs or unknown time Mild brain edema (<10%) Sensitive to Na correction rate Aim to increase Na by 10% (not more than 12 in 24 hrs)
How long has hyponatremia been present?
Does the patient have symptoms?
Does the patient have risk factors for development of neurologic complications?
Monitoring of patients Volume status Daily weight Frequent Serum Na, K Plasma Osmolality Urine Na, K, osmolality Strict Input and Output
Basic concept Free water intake << Free water output
ANDNa, K intake >> Na, K output Needed Info:
Serum Na , osmolality Urine Na, K, Osmolality Strict Input/ Output
Rate of correction
Hyponatremia
Chronic
Asymptomatic
Symptomatic
Long term managementTreat etiologyWater restrictionDemeclocyclineUreaV2 receptor antagonist
Some immediate correctionHypertonic saline + FurosemideChange to water restrictionFrequent serum & urine electrolytesDo not exceed 12 meq/l/d
Emergency Hypertonic saline+ furosemide
Acute <48 hrs Chronic>48 hrs
No immediateCorrection needed
Thurman et al,Therapy in nephrology and Hypertension,Saunders 2003
Treatment based on neurological symptoms and not on Sodium
Needs aggressive management with 3%NaCl
No role of fluid restriction alone Treatment should precede any
neuroimaging Treatment in monitored setting Sodium levels measured every 2 hours
Impending herniation: Sz, resp arrest,, obtundation, Decorticate posturing, dilated pupils:
100 ml of 3% NaCl as a bolus over 10 min to rapidly
reverse brain edema. Repeat bolus as required till symptoms improve
Encephalopathy: Headache, N/V, Altered mental status:
3% NaCl @ 50-100 ml/hr Calculating 3% saline rate: Weight in kg x desired rate of increase in Serum Na
Monitor [Na] every 2-4 hrs Stop active correction when appropriate end point
is reached: Patient becomes asymptomatic Safe Na levels reached (generally 120) Total correction 12 mmol in 24 hrs or 18-20 mmol in 48 hrs Complete rest of correction with - fluid restriction
Attend to underlying cause No immediate correction needed Fluid restriction
Urine Na + K Plasma Na
Recommended water intake
>1 < 500 ml/day
-1 500 to 700 ml/day
< 1 < 1000 ml/day
D Ellison, T Berl. NEJM 2007;356:2064-72
Treatment Mechanism Dose Advantage Limitations Fluid restriction
Decreases availability of free water
Variable EffectiveInexpensive
Non compliance
Encourage dietary salt and protein
Solutes required for free water excretion
Variable
Demeclocycline ↓ ADH response 300-600 mg BID Effective Unrestricted water intake
Nephrotoxic, Polyuria, Photosensitive
V-2 Receptor antagonist -Conivaptan
Antagonize ADH receptor
20-40 mg/dayIV (Vaprisol)
Effective Available only as IV
Take home messageHyponatremia –a common, life threatening problem
In presence of ADH concentrated urine is formed
Treatment – Basic concept: Free water Input << Free water Output Na+K Input >> Na+K Output
Step wise evaluation importantInappropriate treatment – Worse than disease• Practicing is the best way of learning!!!
HyponatremiaAsymptomaticSymptomatic
Long term management
Hypertonic saline
Acute <48 hrsNo immediateCorrection needed
Emergency
Go slow
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