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Module # 26 - Hyponatremia Module
Objectives:
1. List 6 potential causes of hyponatremia.
2. List the diagnostic tests needed to determine the cause of hyponatremia
3. Know maximum amount sodium should be corrected in 24 hours to avoid
complications.
4. Recognize 2 clinical situations where the hyponatremic patient should be monitored in
the ICU.
References:
1. Ellison DH and Berl T. The Syndrome of Inappropriate Antidiuresis. NEJM 2007;
356;20.
2. Fenske W, Maier S, Blechschmidt, Allolio, Stork S. Utility and Limitations fo the
Traditional Diagnostic Approach to Hyponatremia: A Diagnostic Study. The American
Journal of Medicine 2010.
3. Mount D, Krahn T. Hyponatremia: Case Vignettes. Seminars in Nephrology 2009.
4. Moritz M, Ayus C. The Pathophysiology and Treatment of Hyponatremic Encelopathy:
An update. Nephrology Dialysis Transplantation. (2003) 2486-2491.
5. Caramelo C, Molina M, Tejedor A, et al.. Regulation of Postoperative Water Excretion:
A study on Mechanisms. J Am Soc Nephrol (2002).
6. Ayus JC, Wheeler JM, Arieff Al. Postoperative Hyponatremic Encelopahty in
Menstruant Women. Ann Int Med (1992).
Case 1
You are consulted by surgery on a 74 year old male who is 7 days status post bifemoral bypass
and now has a sodium of 121. PMHx is significant for PMR, currently on chronic steroids. At the
time of his admission, his sodium was 138. He was hypotensive intraoperatively and received
multiple fluid boluses in the 48 hours after surgery. Over the past 5 days he is approximately 5
liters negative. The Surgery service has placed the patient on a fluid restriction and gave him 40
mg IV lasix today because they thought his sodium was low from “fluid overload”. On physical
exam he has normal vital signs, is not orthostatic, has moist mucous membranes, axillary sweat,
and has normal skin turgor.
What labs should be checked?
Serum osmolality, Urine osmolality, Ur Na, FENa, uric acid, BUN/Cr ratio, TSH, cosyntropin
stimulation test.
What is on your differential diagnosis?
Hypovolemia vs SIADH (postoperative, drugs, infection, cancer, etc.) vs adrenal insufficiency
are the most likely. Other possibilities include hypothyroidism, renal failure.
Serum osmolality confirms true hyponatremia. Low urine osmolality would suggest an
appropriate response to low osmolality and suggests polydipsia. Urine Na should be low in
hypovolemic hyponatremia, or edematous states. If it is high, it suggests salt-wasting
nephropathy, diuretic therapy, hypoaldosteronism, or occasionally vomiting. It is also high in
SIADH. Uric acid and BUN tend to be low in SIADH and high in hypovolemia.
Results for case:
S osm = 260 mosmol/kg
U osm = 300 mosmol/kg
Ur Na = 40 mEq/L
FENa = 3%
TSH = nl
Stimulation test normal
BUN 15 Cr 1.1
Glu 126 mg/dl
How can we make the distinction?
The urine sodium is often helpful in distinguishing hypovolemic hyponatremia from SIADH. In
SIADH, the Ur Na should be high whereas in hypovolemia, the kidney is actively retaining
sodium and therefore Ur Na should be low. Normal reference range for urine sodium is between
40 and 220 mEq/L. If the diagnosis remains unclear and the urine osmolality is less than 500, it
is safe to give 1-2 liters of normal saline over 48 hours to rule out hypovolemia as the cause. In
true volume depletion, isotonic saline will raise the sodium by 2 mechanisms: it is slightly
hypertonic to plasma, and the increased volume will remove the stimulus to secrete ADH. In
SIADH, the kidney will handle the sodium normally but will retain water because of increased
ADH and impaired urine concentrating ability and lead to little change in the sodium level.
SIADH of unknown etiology is diagnosed. What should be the next step in management?
Begin free water restriction, identify underlying cause and correct. (Review causes of SIADH –
see table 2). Fluid should be restricted to lower than UOP and insensible losses which will lead
to increased osmolality.
What options are available for treatment?
 Loop diuretics- Recommended by some and not others. May be added to NS or hypertonic
saline. The sodium increases solute excretion which allows more water to be excreted. The
loop diuretic acts by inhibiting NaCl reabsorption which leads to increased free water
excretion.
 Sosium, potassium, urea- given as isotonic saline, dietary salt, urea in combination with loop
diuretics. Can be given to patients with true volume depletion or adrenal insufficiency. Urea
acts in similar way but no advantage over sodium.
 Demeclocycline- used in chronic SIADH (takes a week to work). Interferes with ADH action
at renal collecting duct. Significant side effects include nausea, phototoxicity and
azotemia/renal failure.
 Lithium- Similar to demeclocycline but with higher rate of adverse effects, including CNS.
Not generally used.
 Vasopressin-receptor antagonists are a new class of agents that act on the V2 receptor in the
renal collecting duct to inhibit water resorption and induce diuresis. Several clinical trials
have shown these agents to be effective at increasing the serum sodium and increasing free
water clearance, albeit with significant side effects. Conivaptan is currently the only FDA
approved AVP-receptor antagonist (V2 and V1A) for use in euvolemic hyponatremic
patients. It has been shown to increase Na by a mean of 6.9 meq/L at 24 hours. Side effects
are concerning including thirst, infusion site reactions (pH=3.0), hypotension (2.5%), and
overly rapid correction (occurred in 9%). These agents should not be used in patients with
liver disease.
Case 2
A 24 year-old female presents to the ER with altered mental status after a party. In the ER she
has a generalized seizure which is aborted with lorazepam but she remains unresponsive. HR 85,
BP 110/65, O2 sat 98% on 2L NC, BMI 19.
Initial labs show sodium of 115, BUN 20 and Creatinine of 0.8. Weight is 60kg.
What is the initial treatment?
This patient should be treated with hypertonic saline, and have a Renal service consult. Patients
with symptomatic hyponatremia are more likely to be acutely hyponatremic (i.e. developed over
<12 hours) and have a significantly higher mortality rate (50% vs 6%).
Patients with asymptomatic hyponatremia can be managed with fluid restriction and Normal
saline
What is the appropriate level of care for this patient?
MICU. Severe symptomatic hyponatremia (seizures, coma) should be managed in the ICU and
renal service consulted to help manage hypertonic saline infusion.
What consult should be considered to manage this degree of hyponatremia?
Renal
What is the appropriate infusion rate for hypertonic saline in this case?
Male
Female
Elderly Male
Elderly Female
Infusate
Hypertonic (3%)
Saline
Normal (0.9%)
Saline
Lactated Ringers
Total Body Water
(Liters)
Weight (kg) * 0.6
Weight (kg) * 0.5
Weight (kg) * 0.5
Weight (kg) * 0.45
Mmol
Na/Liter
513 mmol/L
154 mmol/L
130 mmol/L
This requires math skills. Various smartphone apps can be helpful here, but
Na Requirement (mmol) = Total Body Water*(Goal Na-Current Na)
Because the patient is symptomatic, the initial goal should be to raise the serum sodium by 3
mmol/L over 3 hours. Sodium should not be corrected more than 8-10 mmol/L in the first 24
hours and not more than 18 mmol/L in the first 48 hours
Na Requirement = (65kg*0.5) (118-115) = 90 mmol. This is the equivalent of .175 L of
Hypertonic Saline (90/513), which given over a 3 hour period about 60cc/hour. The patient’s
sodium can then be corrected more slowly over the next 21 hours, raising it a total of 5 mmol and
using the same math to calculate the rate.
Plasma sodium concentration should be monitored q2-4 hours while receiving hypertonic saline
to ensure patients are not overcorrected.
A simpler strategy? If using 3% Saline, use 1-2 ml/kg/hr to increase serum sodium 12mmol/liter/hour. Use twice this (2-4 ml/kg/hr) to raise sodium more rapidly in patients with
seizure or coma. (0.5 ml/kg/hr) if symptoms are mild.
Name potential causes for this patient’s hyponatremia
Ecstasy (3,4-methylenedioxymethamphetamine [MDMA]) intoxication. A variety of factors
predispose those that use Ecstasy to hyponatremia. First, MDMA can directly affect the
hypothalamus resulting in excessive thirst and polydipsia that may be compounded by rigorous
physical activity (dancing) as may occur at a party. Secondly, MDMA directly induces ADH
excretion, likely compounded by vigorous physical activity resulting in severe inhibition of the
body’s ability to lose water through urination. These effects will impact young thin women more
acutely due to lower muscle mass and decreased TBW compared to men.
Low dietary solute intake, aka Beer Potomania. Malnourshed patients and those that receive
most of their calories from beer have a low solute intake and a high volume intake. The amount
of free water excreted by the kidney depends on the number of osmoles that need to be excreted.
The kidneys can dilute urine to a maximum of 50 mosm/liter, so any additional volume results in
dilution of electrolyte stores.
Other causes to consider- Hypothyroidism, Adrenal Insufficiency.
What if the patient had a glucose level of 654, in addition to the above mentioned sodium of
115?
Glucose acts as an effective osmole in the circulation, drawing water from the intracellular space
into the vasculature. This causes a relative dilution of the circulating sodium concentrations.
Patients are less at risk for cerebral edema seen with other forms of hyponatremia.
Normalization of glucose will allow normalization of intravascular sodium concentrations.
Because it is possible for a patient to be both hyponatremic and hyperglycemic, one must correct
sodium for the degree of hyperglycemia to determine if more than one disorder is present.
Plasma glucose concentrations <400 mg/dl, adjust plasma sodium 1.6 mmol/L for
every 100mg/dl increase in glucose over 100mg/dl.
Plasma glucose >400mg/dl plasma sodium should be corrected by 2.4 mmol/L for
every 100mg/dl increase in glucose over 100mg/dl.
For this patient, 2.4 * 5.5 = 13.2 , so the adjusted sodium is 128.2. The patient has a lesser degree
of hyponatremia but it is still present.
Management should focus on correcting hyperglycemia first and hyponatremia second. This
situation can be tricky, because serum sodium concentrations will correct with normalization of
blood glucose, but use of hypertonic saline would not be appropriate as this could result in
overcorrection of the sodium when serum glucose levels normalize. Very close monitoring of
both blood glucose and sodium levels would be required and this patient would be best cared for
in the ICU.
Post Module Evaluation
Please place completed evaluation in an interdepartmental mail envelope and address to Dr.
Wendy Gerstein, Department of Medicine, VAMC (111) or Dr. Patrick Rendon, UNM Hospital,
Division of Hospital Medicine, 4ACC.
1) Topic of module:__________________________
2) On a scale of 1-5, how effective was this module for learning this topic? _________
(1= not effective at all, 5 = extremely effective)
3) Were there any obvious errors, confusing data, or omissions? Please list/comment below:
______________________________________________________________________________
______________________________________________________________________________
______________________________________________________________________________
______________________________________________________
4) Was the attending involved in the teaching of this module? Yes/no (please circle).
5) Please provide any further comments/feedback about this module, or the inpatient curriculum
in general:
6) Please circle one:
Attending
Resident (R2/R3)
Intern
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