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Hypernatremia - 12/4/2012

posted Dec 4, 2012, 7:16 AM by Rohit Das   [ updated Dec 27, 2012, 6:39 AM by Purnema Madahar ]

Hypernatremia – though overall not as common as its sibling, HYPOnatremia, it is still seen fairly frequently. In one study of critically ill hospitalized patients, hypernatremia (defined as a sodium level of >145 mmol/L) was present at admission in around 10% of patients, and developed during the hospitalization in an additional 3%.  At resident report, we talked about a case of an elderly woman afflicted by a UTI, with bacetermia, who presented with a sodium of 172 – a fairly common situation you’ll see in our fragile and febrile elderly population. 

Before I head into my regular question-based format of talking about things - I wanted to make a clear clinical distinction. Dehydration, i.e. a net free water deficit, IS NOT synonymous with volume depletion. Volume depletion speaks to a pathophysiologic phenomenon where extracellular fluid loss leads to impaired tissue perfusion, and has potential for more advanced hemodynamic compromise (shock). Dehydration can occur WITHOUT volume depletion, and vice versa. Similarly, if extensive, dehydration can LEAD to volume depletion, a scenario we sometimes struggle with from a management standpoint.

Anyway...let’s talk about the following:

·         What are some of the causes of hypernatremia?

·  What are the clinical manifestations, and how do acute and chronic hypernatremia differ?

·         How is hypernatremia appropriately managed?

What are some of the causes of hypernatremia?

·         Hypernatremia represents a body water deficit in relation to the body’s overall sodium stores. This can result from either net water loss, or net sodium gain (e.g., from hypertonic fluid). The former is much more common, as reflected by the case presented today, and that’s what I’ll focus on.

·         Our body’s capability to maintain a normal sodium level is remarkably attuned – a slight increase in plasma osmolality stimulates both ADH secretion and thirst, and this combination allows us to maintain a plasma osmolality within a 1-2% range despite wide variations in water/salt intake.

·         Net water loss and resultant hypernatremia in elderly patients with acute illnesses is multifactorial, and Dr. Lief hit on several key points. First of all, elderly patients with altered cognition have poor access to free water. In one retrospective study of around 100 patients, nearly 90% lacked access to free water. Secondly, elderly patients have an impaired ability to concentrate their urine due to impaired vasculature in the area of the loop of Henle where the interstitial medullary gradient for free water absorption is generated. Finally, urine infections themselves also impair urinary concentrating ability. Taken together, the elderly, demented, bacteria-in-the-bladder ridden patient is EXTREMELY susceptible to hypernatremia.

What are the clinical manifestations, and how do acute and chronic hypernatremia differ?

·         As in hyponatremia, the clinical manifestations are a direct result from osmotic shifts in the brain and consequent cerebral dysfunction. In the context of hypernatremia, brain cells are LOSING water and shrinking, instead of GAINING water and swelling. Also similar to hyponatremia, the severity of the presentation depends on the rapidity of the change in plasma sodium and osmolality.

·         Acute hypernatremia, which is generally defined as occurring over the course of <24 hours, occurs from salt overload as opposed to net water loss. Acute brain shrinking can lead to vascular rupture and intracranial bleeding…and the manifestations are what you’d expect in such a scenario…altered cognition, lethargy, seizures…coma.

·         Chronic hypernatremia is a different situation. As in hyponatremia (feel like I’m writing that a lot...), the brain adapts by shifting non-sodium/potassium active osmoles into cells, thereby normalizing cellular volume. This leads to less marked clinical manifestations as compared to the acute version…

How is hypernatremia appropriately managed?

·         The attached review article goes over the management of hypernatremia succinctly and conceptually. There are really three things to consider—the total water deficit, the rate at which you want to correct, and which fluid you intend on using. Some comments:

·         Depending on what you read, some favor the conventional formula of water water deficit = TBW X (Serum Na/140 – 1) and others don’t. The main gripe is that it most useful with only pure water loss, but underestimates the water deficit in patients with primarily hypotonic fluid loss. The review article uses the formulas displayed on Table 2...whichever way you go, you'll get a decent "guess-timate" of how much free water you'll need to replete before getting the sodium to a normal level.

·         Regarding the rate of correction – the consequences of overly rapid correction are less well defined as compared to hyponatremia, but the theoretical fear is increasing brain volume above normal, leading to cerebral edema and encephalopathy. Based largely on retrospective studies in infants, the recommended rate of correction in chronic hyponatremia is 0.5meQ/L per hour, i.e., 10meQ/L per day. In acute hypernatremia, where cerebral adaptation has not had enough time to allow brain volume to go back to normal, the rate of correction can be more rapid, and recommendations are to decrease the sodium level to normal within 24 hours.

·         The fluid you choose really depends on the clinical context. If there is significant volume depletion, Normal Saline is the first choice. Though it won’t change the plasma sodium significantly, it will also not worsen it, and stabilizing the patient is the priority. Otherwise, hypotonic fluids are used, including ½ NS, D5W most commonly – the more hypotonic the fluid, the less that has to be given. Since potassium also effects plasma osmolality, any K put into fluids for concurrent potassium losses must also be taken into account, as depicted in the formula in Table 2.

Would highly recommend reading the attached review article, I find it pretty useful…

Wow…Match Day tomorrow…Nerve-wracking…may prescribe myself a tiny dose of Ativan…GOOD LUCK EVERYONE!

Adrogue et. al., NEJM 2000 Volume 342(20): 1493-99

12/4/2012 -- Some additional references, courtesy of Dr. Lief

Bhave et. al., Am J Kid Dis 2011, Volume 58 (2): 302-309

Epstein, J Am Soc Neph 1996, Volume 7: 1106-1122

Williams et. al., BMJ 1969, Volume 3: 212-215