Solve hypernatremia with tips and tactics from Dr. Joel Topf, MD (@kidney_boy), our Kashlak Chief of Nephrology. We review the diagnostic workup for hypernatremia, polydipsia and polyuria, review the pathophysiology of diabetes insipidus, and how to differentiate between nephrogenic and central DI. Plus, we walk through how to treat hypernatremia in the acute setting and Dr. Topf shares clinical pearls on why hypernatremia is the opposite of hyponatremia… It’s easy!
Written by Hannah R. Abrams and Joel Topf MD
Producer: Hannah R. Abrams
Cover Art and infographic by: Hannah R. Abrams
Hosts: Hannah R. Abrams; Stuart Brigham MD; Matthew Watto MD, FACP
Editors: Matthew Watto MD, FACP; Emi Okamoto MD
Guest: Joel Topf MD
Hypernatremia is the opposite of hyponatremia: it’s easy. There is no pseudohypernatremia and adult patients will be safe even if you exceed the suggested correction rate of 12 mmol per day (Chauhan 2019).
Patients who can drink water, should be able to protect themselves against hypernatremia. The amount of water they have to drink & urinate may be lifestyle-impeding, though.
In diagnosing hypernatremia, think about why your patient isn’t drinking or why they would be predisposed to losing water, like diarrhea, diuretics, or insensible losses. Don’t forget about the possibility of sodium overload, especially after a code…or a few bottles of soy sauce.
When correcting hypernatremia, think about not only the water the patient must have lost to get to their current sodium (free water deficit), but also their ongoing losses including urine output.
The body has two defenses against hypernatremia: drinking more water and increasing antidiuretic hormone (ADH). Patients who have no ADH (central DI) or can’t respond to ADH (nephrogenic DI) can compensate by drinking extraordinary amounts of water. Thus, their Sodium will often be within the normal range. But, the amount of polyuria and polydipsia can be life-altering and prohibit sleep.
Antidiuretic hormone (ADH, also called vasopressin) is the hormone which responds to increases in osmolality and signals the kidneys to conserve water, principally at the medullary collecting duct. It is made in the hypothalamus and stored in the posterior pituitary.
If the sodium is high, that means the patient has not been able to compensate by drinking water.
Common reasons to be unable to drink water include altered mental status, physical restraints, inability to communicate their need for water, or lack of available water. (Topf 1999)
Patients may have renal losses (due to loop diuretics, osmotic diuresis, or DI) or extrarenal losses (due to insensible losses or diarrhea). Less commonly, sodium overload may be at play: for example, in a patient who received several amps of sodium bicarbonate during a code, massive salt intake (Carlberg 2013) or cutaneous exposure with impaired skin integrity. (Peker 2010, Kaufman 1986)
Think about the ADH axis. In a water deprivation test, the patient is prevented from drinking water for several hours. If urine osmolality fails to rise appropriately– if the body fails to conserve water when it is suddenly withheld– then an absence or functional inability to use ADH exists. At that point give desmopressin (DDAVP), which works in the same way as ADH. If urine osmolality rises, the problem is a lack of ADH (central DI). If it does not, the problem is inability to respond to ADH (nephrogenic DI). (Lavin 2009)
Dr. Topf describes central DI as the body being mute, or unable to make the necessary signal. Think of it as analogous to being unable to make insulin in Type 1 Diabetes. This can be caused by a variety of CNS insults, and may often be idiopathic. (Topf 1999)
The treatment here is the same as the diagnostic: DDAVP. Desmopressin aka DDAVP can be life-changing for these patients; Dr. Topf recalls a patient who told him the first night after starting DDAVP was “the first night [she]’d been able to sleep in weeks” without waking up from thirst. The out-of-pocket cost is about $1 a day.
Dr. Topf describes nephrogenic DI as the body being deaf, or unable to hear the signal no matter how loud. Think of it as similar to insulin resistance in Type 2 Diabetes.
The causes of nephrogenic DI are more complex. They can include congenital causes, acute tubular necrosis (ATN), chronic kidney disease, hypercalcemia, hypokalemia, sickle cell disease, osmotic diuresis, and lithium. (Topf 1999)
Physiologically, furosemide, hypercalcemia, and hypokalemia can cause loss of ADH-triggered water reabsorption. This process relies on a concentrated medullary interstitium for water to flow into: ADH can open the door, but something has to pull the water through. Hypercalcemia and hypokalemia each inhibit the thick ascending limb of the loop of Henle from making that gradient. (Topf 1999) Chronic treatment depends on the cause of nephrogenic DI.
In the acute setting, treat hypernatremia by replacing the missing water, either orally (preferred) or by D5W if the patient is unable to drink and does not have an enteral tube (NG tube, PEG, etc.). For patients who are both hypovolemic and hypernatremic, Dr. Topf recommends running both maintenance fluids and D5W.
Dr. Topf recommends his “Yesterday, Today, Tomorrow” framework for calculating the correction rate. This refers to adding up the water losses from yesterday and today to generate the target water intake for tomorrow.
Calculate the fluid deficit, or the water that the patient has already lost to get to their current sodium. There are several formulas, but Dr. Topf recommends the following (Note: See below for information on setting a target Na):
First, determine how much the sodium is elevated relative to target (as a percentage):
(Current Na – Target Na)/Target Na
Multiply that by the total body water. Dr. Topf recommends estimating 60% body water for lean/younger men, 50% for lean/younger women and older men, and 45% for older women. The full formula for water deficit:
(% Body Water x Body Weight) x [(Current Na – Target Na)/Target Na]
Calculating the ongoing fluid losses, how much free water the patient is losing daily as you replete. Dr. Topf recommends the following shortcut:
Kashlak Pearl: For first 1L urine, ignore. For urine output (UOP) between 1-3L, assume half of this UOP is lost free water. Assume all UOP beyond 3L is completely lost as free water.
The more precise method is the electrolyte free water clearance:
Urine volume x (1- (Urine Na + Urine K) / serum Na)
Add ‘Yesterday’ and ‘Today’ to find the target water intake for ‘Tomorrow’. Dr. Topf recommends dividing by 24 hours and giving hourly as oral free water (preferred) or D5W if the patient is unable to drink or does not have an NG tube. NOTE, large volumes of D5W may cause osmotic diuresis (through hyperglycemia) and worsen renal water losses.
10-12 mmol/day is a commonly used target rate for correction of hypernatremia, and a recent study showed no evidence that more rapid correction was associated with greater risk of mortality, cerebral edema, or adverse events (Chauhan 2019). In contrast, there are risks for overcorrecting hyponatremia (central pontine myelinolysis) and also for individuals like marathon runners who acutely develop hyponatremia (cerebral edema).
Free water and D5W distribute in the body, and Dr Topf notes only ~10% volume remains in plasma, with majority moving intracellularly (two thirds) and the rest distributing in the interstitium. Note this is different than isotonic fluids, like normal saline, which will contribute to volume overload.
Thiazide diuretics in combination with a low salt diet have long been used to treat nephrogenic DI due to lithium. However, more recent literature suggests that acetazolamide may also be effective, and may be effective for patients whose nephrogenic DI is refractory to thiazides. (Gordon 2016)
Listeners will recall the pathophysiology of hypernatremia and develop an approach to diagnosis and management of hypernatremia, polyuria, and polydipsia in various practice settings.
After listening to this episode listeners will…
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Dr Topf lists the following disclosures on his website: “I have an ownership stake in a few Davita run dialysis clinics and a vascular access center. Takeda Oncology made a donation to MM4MM the program that is taking me to Mount Everest in 2018”. The Curbsiders report no relevant financial disclosures.
Topf J, Abrams HR, Brigham SK, Okamoto E, Watto MF. “170 Hypernatremia is Easy with Joel Topf MD”. The Curbsiders Internal Medicine Podcast. http://thecurbsiders.com/episode-list. September 2, 2019.
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