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Hypernatremia Primary Care Conference K. Mae Hla, M.D., M.H.S. April 21, 2004 Objectives • Brief review of pathophysiology, causes, clinical manifestations of hypernatremia • Review management, emphasizing a quantitative approach to correction of fluid imbalance Disclosure Not sponsored by any pharmaceutical companies The Patient • 51-year-old male with acutely decompensated schizo-affective disorder was readmitted 1 day after discharge to UW Psychiatry involuntarily for increasing agitation and psychosis • History of noncompliance with medications (Lithium 1200 mg, Clozaril 375 mg, Modafinil 400 mg, Synthroid 75 mcg) all of which were restarted Deterioration during hospitalization • Patient was in and out of locked seclusion due to violent behavior with subsequent poor oral intake • CBC, Chem 7 and CK were done after 4 days because staff felt that patient’s mental status has worsened and dystonia might be present • Serum sodium was noted to be high, and a general medicine consult was requested Physical Exam • BP: 160/82, P: 92, T: 37; orthostatic to 110/60 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 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 What is the cause of his hypernatremia? Water homeostasis • Water homeostasis is mediated by: – Thirst – Arginine Vasopressin (ADH) – Kidneys • A disruption in the water balance leads to abnormality in serum sodium Hypernatremia (Na+ > 145 mEq) • Hypernatremia is caused by a relative deficit 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 Extracellular-Fluid & Intracellular-Fluid Compartments under Normal Conditions and during States of Hypernatremia 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 Pure Water Loss (cont’d) • 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 V2receptor antagonists) Causes of Hypernatremia (cont’d) Hypotonic fluid loss • Renal causes Loop diuretics Osmotic diuresis (glucose, urea, mannitol) Postobstructive diuresis Polyuric phase of acute tubular necrosis Intrinsic renal disease Hypotonic Fluid Loss (cont’d) • Gastrointestinal causes Vomiting Nasogastric drainage Enterocutaneous fistula Diarrhea Use of osmotic cathartic agents (e.g., lactulose) • Cutaneous causes Burns Excessive sweating Causes of Hypernatremia (cont’d) Hypertonic sodium gain Hypertonic sodium bicarbonate infusion 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 What is the hypernatremia due to in our patient? • Poor water/oral intake due to psychosis (per hx) • Acquired partial nephrogenic DI due to Lithium (suggested by low urine osmolality relative to high serum osmolality) • Increased insensible loss due to agitation, and hyperventilation • ?? Renal loss of sodium-urine Na+ 41 Clinical Manifestations • CNS dysfunction s/s depend on large or rapid increases 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 Management A two-pronged approach: • Addressing the underlying cause: stopping GI loss, controlling pyrexia, hyperglycemia, correcting hypercalcemia or feeding preparation, moderating lithium induced polyuria • Correcting the prevailing hypertonicity: rate of correction depends on duration of hypernatremia to avoid cerebral edema Effects of Hypernatremia on the Brain and Adaptive Responses Correction of Hypernatremia • Hypernatremia that developed over a period of hours (accidental loading) – Rapid correction improves prognosis without cerebral edema – Accumulated electrolytes in brain rapidly extruded – Reducing Na+ by 1 mmol/L/hr appropriate Rate of Correction (Cont’d) • Hypernatremia of prolonged or unknown duration – a slow pace of correction prudent – full dissipation of brain solutes occurs over several days – maximum rate 0.5 mmol/L/hr to prevent cerebral edema – A targeted fall in Na+ of 10 mmol/L/24 hr Goal of Treatment • Reduce serum sodium concentration to 145 mmol/L • Make allowance for ongoing obligatory or incidental losses of hypotonic fluids that will aggravate the hypernatremia • In patients with seizures prompt anticonvulsant therapy and adequate ventilation Administration of Fluids • Preferred route: oral or feeding tube • IV fluids if oral not feasible • Except in cases of frank circulatory compromise, isotonic saline is unsuitable • Only hypotonic fluids are appropriate-pure water, 5% dextrose, 0.2 % saline, 0.45% saline-the more hypotonic the infusate, the lower the infusion rate required Calculation of Free Water Deficit Assuming pure water loss, CBW x [Na+] = NBW x 140 NBW = (CBW x [Na+]) / 140 Water 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 Patient’s Serial Electrolytes Before and After Treatment 4/22 Na+ K Cl CO2 BUN Creat Glu 145 4.5 110 25 17 1.1 87 4/26 154 4.8 114 29 28 1.4 4/27 4/27 (a.m.) (p.m.) 150 154 4.4 4.8 115 117 26 26 27 25 1.4 1.4 100 92 Formula for Managing Hypernatremia CLINICAL USE FORMULA* infusate Na+ - serum Na+ 1. Change in serum Na+ = total body water + 1 Estimate the effect of 1 liter of any infusate on serum Na+ (infusate Na+ + infusate K+) -serum Na+ 2. Change in serum Na+ = total body water + 1 Estimate the effect of 1 liter of any infusate containing Na+ and K+ on serum Na+ Characteristics of Infusate Infusate 5% Dextrose in H20 Infusate Na+ Extracellular-Fluid Distribution mmol per liter % 0 40 0.2% NaCl in 5% dextrose in H2O 34 55 0.45% NaCl in H2O 77 73 Ringer’s lactate 130 97 0.9% NaCl in H2O 154 100 Rate of infusion of 0.2 saline in 5% dextrose in water Change 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/L over 24 hours Thus needs 9/3 = 3 L (over 24 hours) Calculated rate of infusion = 3000/24 = 125 ml/hr Change in Serum Na+ after adjusting the infusate and rate 4/22 4/26 Na+ K Cl CO2 BUN Creat Glu 145 4.5 110 25 17 1.1 87 154 4.8 114 29 28 1.4 4/27 4/27 4/28 4/28 (a.m.) (p.m.) (a.m.) (p.m.) 150 154 151 148 4.4 4.8 4.2 3.7 115 117 115 114 26 26 26 26 27 25 23 20 1.4 1.4 1.3 1.3 100 92 115 115 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 pt’s clinical status and electrolyte values