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  • 8/3/2019 Hla Hyper Nat Re Mia Handout

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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