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Deranged Physiology » Required Reading » Electrolytes and fluids
Hyponatremia: a lazy man's classification
Historically, the college has asked specifically about the diagnostic approach to hyponatremia in the
following SAQs:
estion 24 from the first paper of 2016 (classification of hyponatremia, as well as management)
estion 12.2 from the second paper of 2014: " Briefly outline how you will determine the
underlying cause" of a hyponatremia in a post-op patient with a history which offers multiple
possible explanations of hyponatremia
estion 14 from the first paper of 2005 (approach to diagnosis and sodium replacement)
estion 7 from the second paper of 2002 (essentially identical to estion 14 from the first
paper of 2005)
Actual case studies of hyponatremia have included the following questions:
estion 20.4 from the second paper of 2015 - pseudohyponatremia, with high triglycerides
estion 21 from the second paper of 2009 - isoosmolar hyponatremia; "TURP syndrome"
estion 7.3 from the second paper of 2013 - water intoxication due to bowel prep
estion 14.3 from the first paper of 2009 - water intoxication due to beer potomania
estion 3 from the second paper of 2007 - sodium loss due to effects of mannitol diuresis
estion 30.1 from the first paper of 2014 - hyponatremia in hypothyroidism due to amiodarone
estion 29 from the first paper of 2015 - lots of detail about SIADH
estion 20.1 from the first paper of 2013 - hyponatremia in head injury
estion 5.1 from the second paper of 2011 - indapamide-induced hyponatremia
estion 14.4 from the first paper of 2009 - SIADH, and the calculation of sodium deficit
Anthony Delaney and Simon Finfer wrote the fluid and electrolyte chapter for Oh's Manual (Ch.93, p.
949). One expects that at some stage these people may have wrien some of the past paper questions.
At this, one might conclude that a thorough knowledge of that chapter would therefore be of interest
to the more cunning candidate. To some extent, this is true. Of specific interest is Box 93.1 ("Common
causes of hyponatremia") on page 952. In homage to Oh's manual, Box 93.1 is reproduced below with
minimal processing (only a few additions).
Finfer and Delaney's chapter for Ohs Manual does not enter into over-long discussions of volume
status, perhaps tacitly acknowledging that we suck at determining it. eir classification resembles
neither the classical paern, nor the lazy man's shortcut seen below. Rather, they separate
hyponatremia into "spurious" (i.e. due to some sort of error), "water retaining" (which includes heart,
liver and kidney failure, SIADH and polydipsia) and "salt losing" (a minority group including diuretic
excess and hypoadrenalism).
As for the diagnosis of hyponatremia, the Manual is somewhat lacking. A brief discussion of tonicity as
a classification system for hyponatremia is followed by an indepth exploration of only three specific
hyponatremias: TURP syndrome, SIADH and cerebral salt wasting. e Manual's concentrated wisdom
was expanded upon in specific chapters relevant to these disease states:
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TURP syndrome is visited in the chapter on isoosmolar hyponatremia
SIADH has its own dedicated chapter
Cerebral salt wasting has its own dedicated chapter
e best resource for hyponatremia is probably the 2002 article by Haralampos Milionis. It offers a
step-by-step diagnostic algorithm (which was used as a model for the ones in this chapter) and
discusses the diagnostic pathway with just enough detail. LITFL also have a page on this in the CCC,
and it too offers a diagnostic algorithm.
Classification of hyponatremia
In essence this approach relies on the clinician's abilities of assessing volume. ere is an alternative,
seen below. Notice how at no stage is one invited to actually examine the patient. No, it does not
include the usual "hypervolemic, hypovolemic, normovolemic" classification. For one, clinicians are
very poor at detecting all but the grossest fluid balance disturbances. And ultimately, I wanted a
diagnostic algorithm which one could use to narrow down the list of differentials over the phone.
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A lazy man's classification of hyponatremia
Diagnostic approach to hyponatremia
ere are two possible approaches to the diagnosis of hyponatremia: . Both are offered here. In their
most basic form, the classical method and the "lazy man's method" require essentially the same tests
(serum osmolality, urine osmolality and urinary sodium). In the classical method, one is expected to
examine the patient and come to a conclusion regarding their fluid status. e lazy man will of course
do no such thing, as it requires for him to get up. Instead, the examination of the patient is deferred
until the absolute last moment, and consists of deciding whether the patient has SIADH or cerebral salt
wasting.
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Causes of Hyponatremia
Spurious result
Water retention
Iso-osmolar
High urine sodium
High triglycerides
High serum protein
Glycine (TURP
syndrome)
Hyper-osmolar
Sodium excretion
Renal failure
Diuretics (but not
enough!)
SIADH
Post-ATN diuresis
Hypoaldosteronism
Diuretic excess
Cerebral salt wasting
Inappropriate fluid replacement (5%
dex)
Low urine sodium
Hyperglycaemia
Psychogenic polydipsia
Mannitol
True hypovolemia
Sorbitol
Cirrhosis
Maltose
Congestive cardiac failure
Radiocontrast dye
Of specific interest to the exam candidate is SIADH. is comes up frequently, and was the topic of a
particularly in-depth SAQ (estion 29 from the first paper of 2015) which was only passed by 29% of
the candidates. SIADH is explored in
History in hyponatremia
e following bits of historical information are important:
Medication history (diuretics, steroids, drugs which cause SIADH eg. SSRIs)
Fluid chart (has somebody been mindlessly charting dextrose)
Psychosocial history (is psychogenic polydipsia even a possibility; are they on a weird diet)
Alcohol history (liver disease, cirrhosis, beer potomania)
Oedema history (Ascites worse recently? Sleep on twenty pillows?)
Trauma history (cerebral salt wasting, pituitary injury)
Urine output (massive diuresis of HONK or ATN recovery phase, or oliguria or chronic renal
failure)
Recent procedures: TURP, contrast CT, recent surgery, etc.
Investigations in hyponatremia
e following standard baery of tests can be launched; particularly if history is unhelpful, or one
cannot bring oneself to interview the patient or their family.
In brief:
Essential tests:
Serum osmolality
Urine osmolality
Urinary sodium
Optional tests:
ABG
Serum triglycerides
Serum protein level
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TFTs
LFTs
Urea and creatinine
Random cortisol
Short synacthen test
Serum osmolality in hyponatremia
is is always asked for, as it helps classify the hyponatremia as "something-osmolar", i.e. isoosmolar
or hyperosomolar. However, realistically in most circumstances one may safely dispense with this
investigation. Even when answering the phone at night, you would know whether the patient has had
a TURP in the last 24 hours, or whether they are suffering from a hyperosmolar coma. Serum
osmolality is mainly a screening test for isoosmolar hyponatremia, as it may reveal an extremely high
serum protein or lipid. Outside of those scenarios, the serum osmolality is usually boring and low.
So, prey much all the hyponatremia you're ever going to deal with is going to be hypoosmolar.
Urine osmolality in hyponatremia
is is also ordered frequently, and also has low yield. A thorough exploration of urine osmolality (and
specific gravity, and why they aren't interchangeable) is carried out in the chapter on urinary
electrolytes. In brief, this investigation helps you decide whether or not the kidneys have retained their
ability to make dilute urine. Producing copious amounts of dilute urine is the only sensible way you
can physiologically restore your tonicity, short of engaging in high-risk sodium seeking behaviour.
Ergo, a hypoosmolar hyponatremic person should pee buckets, and their urine should resemble tap
water.
A maximally dilute urine (around 50-100 mOsm/L) suggests that the normal mechanisms in defence of
tonicity are intact; i.e. vasopressin release has been appropriately suppressed. is is a characteristic of
the following hyponatremias:
Psychogenic polydipsia (Oh's Manual suggests that about 15-20L of water need to be consumed
every day before one actually develops hyponatremia from this)
Beer potomania (as well as anorexia nervosa, or strange diets chronically devoid of sodium)
Inappropriate IV fluid
Dilute urine may also be the consequence of pathological states where the concentrating capacity is
impaired, i.e. irrespective of what the posterior pituitary is doing the kidneys simply cannot produce
anything but dilute urine.
Post-obstructive diuresis
e polyuric phase of acute tubular necrosis
Diuretic use (although osmolality may be higher than 100mOsm/kg)
Additonally, dilute urine with hyponatremia may be produced in cases of a "reset osmostat", where the
homeostatic setpoint for serum osmolality is depressed. So, a low urine osmolality narrows the
differentials very significantly. However, urine which remains obstinately concentrated in spite of a
hypoosmolar state is not informative, as it leads to a massive number of differentials. e urinary
sodium is the investigation of choice to help discriminate among them.
Urine sodium in hyponatremia
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is investigation on its own only tells you what the renal sodium handling capacity is like. is has a
fairly peripheral importance to the sodium disturbance. Jack Orloff et al (1959) in their clinical
conference on hyponatremia remarked:
"Perhaps the main source of confusion regarding this syndrome has been the lack of
appreciation of the basic fact that the concentration of sodium in the extracellular fluid is
largely determined by the relationship between the intake and excretion of water, rather than
by the relationship between the intake and output of salt."
Correctly, the output of salt has lile to do with the situation. Many hyponatremic patients have an
excess of sodium (eg. oedematous cardiac failure patients). e normal response to hyponatremia is to
retain as much sodium as possible, and therefore a high urine sodium in the face of serum
hyponatremia suggests that there is some sort of sodium wasting disorder taking place, but these are
uncommon. Causes of hyponatremia with a high urine sodium include the following:
Hypoadrenalism
Hypothyroidism
Acute or chronic renal failure
SIADH
Cerebral salt wasting
Post-obstructive diuresis
e polyuric phase of acute tubular necrosis
Diuretic use
Urinary sodium is most useful when one needs to discriminate between SIADH and dehydration.
Dehydration is a syndrome of "appropriate" ADH secretion - it is correct to oppose diuresis if you are
volume-depleted. In such a situation, aldosterone secretion also increases and sodium reabsorption
takes place, leading to a urinary sodium around 10mmol/L (which is the theoretical minimum).
Generally speaking, anything less than 20mmol/L is thought to be an appropriate sodium-conserving
gesture when you are in a hypovolemic state. In contrast, SIADH is an euvolemic state, and the urinary
sodium is usually normal or high (the usual diagnostic criteria specify a threshold value for urinary
sodium, over 40mmol/L.)
us, if urinary sodium is low, it could represent a normal renin-angiotensin-aldosterone response to
hypovolemia, or an abnormal overreaction to an "apparent" low volume state. Differentials include the
following:
Heart failure
Advanced cirrhosis
Nephrotic syndrome
True hypovolemia, eg. following massive haemorrhage
Urine sodium can also be low in situations were the renal sodium and water handling is completely
intact, in which case it represents a perfectly reasonable aempt to retain sodium and excrete excess
water. Psychogenic polydipsia, beer potomania and excessive 5% dextrose administration are possible
causes of such a scenario.
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Previous chapter: Hypertonic saline in critical
care
Next chapter: Hyperosmolar hyponatremia
References
Chung HM, Kluge R, Schrier RW, Anderson RJ. Clinical assessment of extracellular fluid volume in
hyponatremia. Am J Med. 1987 Nov;83(5):905-8.
Milionis, Haralampos J., George L. Liamis, and Moses S. Elisaf. "e hyponatremic patient: a systematic
approach to laboratory diagnosis."Canadian Medical Association Journal 166.8 (2002): 1056-1062.
Shapiro, Michael D., and Stuart L. Linas. "Sodium chloride pica secondary to iron-deficiency anemia."
American Journal of Kidney Diseases 5.1 (1985): 67-68.
ORLOFF, JACK, et al. "Hyponatremia." Circulation 19.2 (1959): 284-299.
Rothenberg, David M., Arnold S. Berns, and Anthony D. Ivankovich. "Isotonic hyponatremia following
transurethral prostate resection." Journal of clinical anesthesia 2.1 (1990): 48-53.
Ayus, J. Carlos, and Allen I. Arieff. "Glycine-induced hypo-osmolar hyponatremia." Archives of internal
medicine 157.2 (1997): 223-226.
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