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

DisclosureNot 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 lossPure 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 hypokalemiaDrugs (lithium, demeclocycline, foscarnet,

methoxyflurane, amphotericin B, vasopressin V2-receptor 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 causesVomiting

Nasogastric drainage

Enterocutaneous fistula

Diarrhea

Use of osmotic cathartic agents (e.g., lactulose)

• Cutaneous causesBurns

Excessive sweating

Causes of Hypernatremia (cont’d)

Hypertonic sodium gainHypertonic sodium bicarbonate infusionIngestion of sodium chlorideIngestion of sea waterSodium chloride-rich emeticsHypertonic saline enemasIntrauterine injection of hypertonic salineHypertonic sodium chloride infusionHypertonic dialysisPrimary hyperaldosteronismCushing’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 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

Formula for Managing Hypernatremia

CLINICAL USE

Estimate the effect of 1 liter of any infusate on serum Na+

Estimate the effect of 1 liter of any infusate containing Na+ and K+ on serum 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

Characteristics of Infusate

Infusate Infusate Na+

Extracellular-Fluid Distribution

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

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 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

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