hla hyper nat re mia handout
TRANSCRIPT
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Hypernatremia
Primary Care Conference
K. Mae Hla, M.D., M.H.S.April 21, 2004
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Objectives
Brief review of pathophysiology, causes,clinical manifestations of hypernatremia
Review management, emphasizing aquantitative approach to correction offluid imbalance
DisclosureNot sponsored by any pharmaceutical companies
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The Patient
51-year-old male with acutely decompensatedschizo-affective disorder was readmitted 1 day
after discharge to UW Psychiatry involuntarilyfor increasing agitation and psychosis
History of noncompliance with medications(Lithium 1200 mg, Clozaril 375 mg, Modafinil400 mg, Synthroid 75 mcg) all of which wererestarted
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Deterioration during
hospitalization
Patient was in and out of locked seclusion
due to violent behavior with subsequent poororal intake
CBC, Chem 7 and CK were done after 4 daysbecause staff felt that patients mental status
has worsened and dystonia might be present Serum sodium was noted to be high, and a
general medicine consult was requested
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Physical Exam
BP: 160/82, P: 92, T: 37; orthostatic to110/60 previous evening per nursing note
Tongue and oral mucosa: dry Skin: poor turgor and tenting
Cor: JVP-flat, normal heart sounds
Lungs: Clear. Abdomen, non-tender, BS + GU: incontinent of urine in diaper
Neuro: limited exam, incoherent, psychotic,agitated, in 4 point leather restraints
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Initial Lab Results
Sodium = 154
Potassium = 4.4
Chloride = 115 HCO3 = 26
BUN = 27
Creatinine = 1.4
Calcium = 10.1
Glucose = 100
Urine Na+ = 41 Urine Osmolality = 492
Plasma Osmolality = 315
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What is the cause of his
hypernatremia?
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Water homeostasis
Water homeostasis is mediated by:
Thirst
Arginine Vasopressin (ADH)
Kidneys
A disruption in the water balance leads
to abnormality in serum sodium
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Hypernatremia (Na+ > 145 mEq)
Hypernatremia is caused by a relativedeficit of water in relation to sodium
which can result from Net water loss: accounts for majority of
cases of hypernatremia pure water loss
hypotonic fluid loss Hypertonic gain results from iatrogenic
sodium loading
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Extracellular-Fluid & Intracellular-Fluid Compartments underNormal Conditions and during States of Hypernatremia
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Causes of Hypernatremia
Net water loss
Pure water loss
Unreplaced insensible losses (dermal and respiratory)
Hypodipsia
Neurogenic diabetes insipidus Post-traumatic
tumors, cysts, histiocytosis, tuberculosis, sarcoidosis
Idiopathic
aneurysms, meningitis, encephalitis, Guillain-Barre
syndrome
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Pure Water Loss (contd)
Congenital nephrogenic diabetes insipidus
Acquired nephrogenic diabetes insipidus
Renal disease (e.g. medullary cystic disease)Hypercalcemia or hypokalemia
Drugs (lithium, demeclocycline, foscarnet,methoxyflurane, amphotericin B, vasopressin V2-
receptor antagonists)
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Causes of Hypernatremia (contd)
Hypotonic fluid loss
Renal causes
Loop diuretics
Osmotic diuresis (glucose, urea, mannitol)
Postobstructive diuresis
Polyuric phase of acute tubular necrosis
Intrinsic renal disease
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Hypotonic Fluid Loss (contd)
Gastrointestinal causes
Vomiting
Nasogastric drainage
Enterocutaneous fistula
Diarrhea
Use of osmotic cathartic agents (e.g., lactulose)
Cutaneous causesBurns
Excessive sweating
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Causes of Hypernatremia (contd)
Hypertonic sodium gainHypertonic sodium bicarbonate infusion
Ingestion of sodium chloride
Ingestion of sea water
Sodium chloride-rich emeticsHypertonic saline enemas
Intrauterine injection of hypertonic saline
Hypertonic sodium chloride infusion
Hypertonic dialysisPrimary hyperaldosteronism
Cushings syndrome
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What is the hypernatremia
due to in our patient? Poor water/oral intake due to psychosis
(per hx)
Acquired partial nephrogenic DI due toLithium (suggested by low urine osmolalityrelative to high serum osmolality)
Increased insensible loss due to agitation,and hyperventilation
?? Renal loss of sodium-urine Na+ 41
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Clinical Manifestations
CNS dysfunction s/s depend on large or rapidincreases in serum Na+ concentration
Outpatients: Affects extremes of ages
Infants: hyperpnea, restlessness, m/s weakness,lethargy, coma
Elderly: few sx until Na+ > 160; confusion, coma
more related to coexisting condition Inpatients: all ages, sx more elusive in presence
of pre-existing neurologic dysfunction
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Management
A two-pronged approach:
Addressing the underlying cause: stopping
GI loss, controlling pyrexia, hyperglycemia,correcting hypercalcemia or feedingpreparation, moderating lithium inducedpolyuria
Correcting the prevailing hypertonicity: rateof correction depends on duration ofhypernatremia to avoid cerebral edema
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Effects of Hypernatremia on the Brain andAdaptive Responses
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Correction of Hypernatremia
Hypernatremia that developed over aperiod of hours (accidental loading)
Rapid correction improves prognosiswithout cerebral edema
Accumulated electrolytes in brain rapidly
extruded Reducing Na+ by 1 mmol/L/hr appropriate
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Goal of Treatment
Reduce serum sodium concentration to145 mmol/L
Make allowance for ongoing obligatoryor incidental losses of hypotonic fluidsthat will aggravate the hypernatremia
In patients with seizures promptanticonvulsant therapy and adequateventilation
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Administration of Fluids
Preferred route: oral or feeding tube
IV fluids if oral not feasible
Except in cases of frank circulatorycompromise, isotonic saline is unsuitable
Only hypotonic fluids are appropriate-pure
water, 5% dextrose, 0.2 % saline, 0.45%saline-the more hypotonic the infusate, thelower the infusion rate required
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Calculation of Free Water Deficit
Assuming pure water loss,
CBW x [Na+] = NBW x 140
NBW = (CBW x [Na+
]) / 140Water deficit = NBW CBW
= {CBW x [Na+] / 140} CBW
= CBW {[Na+] / 140} 1}
= 65 x 0.6 x (154/140 1)
= 39 x (14/140)
= 3.9 L
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Patients Serial Electrolytes
Before and After Treatment
4/22 4/26 4/27(a.m.)
4/27(p.m.)
Na+ 145 154 150 154
K 4.5 4.8 4.4 4.8
Cl 110 114 115 117
CO2 25 29 26 26
BUN 17 28 27 25
Creat 1.1 1.4 1.4 1.4
Glu 87 100 92
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Formula for ManagingHypernatremia
CLINICAL USE
Estimate the effect of 1 liter of any
infusate on serum Na+
Estimate the effect of 1 liter of anyinfusate containing Na+ and K+ onserum Na+
FORMULA*
1. Change in serum Na+
=
2. Change in serum Na+ =
infusate Na+ - serum Na+
total body water + 1
(infusate Na+ + infusate K+) -serum Na+
total body water + 1
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Characteristics of Infusate
Infusate Infusate Na+
Extracellular-FluidDistribution
mmol per liter %
5% Dextrose in H20 0 40
0.2% NaCl in 5% dextrose in H2O 34 55
0.45% NaCl in H2O 77 73
Ringers lactate 130 97
0.9% NaCl in H2O 154 100
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Rate of infusion of 0.2 saline
in 5% dextrose in waterChange in Na+ with 1 L of above solution
= (34-154) / {(65 x 0.6) + 1} = -120/40 = - 3 mEq/L
Desired change in Na+ = 145 154 = - 9 mEq/Lover 24 hours
Thus needs 9/3 = 3 L (over 24 hours)
Calculated rate of infusion = 3000/24 = 125 ml/hr
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Change in Serum Na+ afteradjusting the infusate and rate
4/22 4/26 4/27(a.m.)
4/27(p.m.)
4/28(a.m.)
4/28(p.m.)
Na+ 145 154 150 154 151 148
K 4.5 4.8 4.4 4.8 4.2 3.7
Cl 110 114 115 117 115 114
CO2 25 29 26 26 26 26
BUN 17 28 27 25 23 20
Creat 1.1 1.4 1.4 1.4 1.3 1.3
Glu 87 100 92 115 115
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Summary of Managing
Hypernatremia Isotonic saline unsuitable except in ECF volume
depletion causing hemodynamic instability
Switch to hypotonic solutions as soon as
circulatory status stabilized Avoid excessive rapid correction or over
correction
Select the most hypotonic infusate suitable with
appropriate allowances for ongoing fluid losses Most important - reassess infusion prescriptions
at regular intervals based on pts clinical statusand electrolyte values