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 • Calcium = 10.1
• Potassium = 4.4 • Glucose = 100
• Chloride = 115 • Urine Na+ = 41
• HCO3 = 26 • Urine Osmolality = 492
• BUN = 27 • Plasma Osmolality = 315
• Creatinine = 1.4
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 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 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 4/26 4/27 4/27
(a.m.) (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
FORMULA* CLINICAL USE

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

1. Change in serum Na+ = total body water + 1 infusate on serum Na+

(infusate Na+ + infusate K+) -serum Na+

2. Change in serum Na+ = Estimate the effect of 1 liter of any
total body water + 1
infusate containing Na+ and K+ on
serum Na+
 Characteristics of Infusate
Extracellular-Fluid
Infusate Infusate Na+ 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 4/27 4/28 4/28
(a.m.) (p.m.) (a.m.) (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