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Discussion Starter · #1 ·
A 62 year old man with advanced cirrhosis is treated with lactulose for hepatic encephalopathy. On physical examination he is confused and has asterixis. Blood pressure is 100/60 while the patient is supine and his pulse rate is 110 beats per minute. There is no peripheral edema, but ascites is detected. Serum sodium concentration is 160 mmol/L and potassium is 2.6 mmol/L. The body weight is 64 kg.

This patient's hypernatremia can be best described by which of the following?

A. Excessive insensible losses, primarily of water (euvolemic hypernatremia)
B. Hypotonic losses of sodium and potassium and water (hypovolemic hypernatremia)
C. Hypervolemic hypernatremia
D. Not enough information to determine status
E. None of the above

??????????
 

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B. Hypotonic losses of sodium and potassium and water (hypovolemic hypernatremia)

lactulose therapy is associated with hypernatremia and hypokalemia...
as lactulose increases fluid loss from intestine that is rich in potessium n water but poor in sodium...leading to contraction of extracellular fluid....n hypermatremia....

hepatic encephalopathy itself contribute to it...as pt's oral intake of water is also decreased...
 

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Yes looks like B.

Hypotonic losses of sodium and potassium and water (hypovolemic hypernatremia)
 
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Answer C

Cirrhosis results in portal hypertension and there is significant pooling of blood in splancnic circulation. There is reduced blood flow to kidneys resulting in hyperaldosterinism (secondary). Hence hypernatremia with hypokalemia and hypervolemia. The apparent hypovolemia suggested by the supine hypotension is probably due to the sequestration of fluid in the interstitium (ascites, edema). Am not 100 % sure of my answer.
 

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A is correct!

i think it may due to overuse of lactulose which can result in severe diarrhea ,so dehydration with more loss of water than sodium .
 

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There is no Lactulose overdosage here

There is no points mentioned in the Q that suggests there has been diarrhea in excess to what is expected in lactulose therapy. Since the patients signs of hepatic encephalopathy have not regressed it may even be assumed that the dosage was not enough. So lets concentrate on the cirrhosis than lactulose.
 

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Remember.. hyperaldosterinism is more important than hypoalbuminemia in cirrhosis induced ascites

Portal hypertensive ascites is initiated by altered hepatic and splanchnic hemodynamics, which cause transudation of fluid into the interstitial space. When the rate of interstitial fluid formation exceeds the lymph drainage capacity, ascites accumulates. This pathophysiologic process results in an intravascular volume deficit, which initiates compensatory mechanisms such as aldosterone secretion, to restore plasma volume. Both the liver and intestines are important sites of ascites formation, and clinically significant ascites is rare in patients with extrahepatic portal hypertension. The hypoalbuminemia that often accompanies advanced chronic liver disease may also contribute to ascites formation...

Reference from
McPherson & Pincus: Henry's Clinical Diagnosis and Management by Laboratory Methods
 

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it could be C too....:redcheeks;
if we consider live failure...liver unable to metabolize aldosterone...secondary hyperaldosteron....more sodiun retension....so Hypervolemic hypernatremia....
 

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A 62 year old man with advanced cirrhosis is treated with lactulose for hepatic encephalopathy. On physical
examination he is confused and has asterixis. Blood pressure is 100/60 while the patient is supine and his pulse
rate is 110 beats per minute. There is no peripheral edema, but ascites is detected. Serum sodium concentration is
160 mmol/L and
.. come on pls put up the answer:sorry:
 

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actually there r 3 reasons for hypernatremias...
1 hyperaldosteronism due to liver failure...
2 lectulose
3 hypotension stimulating renin angiotensin system....

hmm...lectulose can be ruled out...if its not in high doses...
n as the pt has only ascites...not the peripheral edema...hmmm...ascites alone is not sufficient to cause hypotension..n stimulate renin secretion....is it?
so remained only option with liver failure....:)
so now m with C Hypervolemic hypernatremia
 

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A small correction

it could be C too....:redcheeks;
if we consider live failure...liver unable to metabolize aldosterone...secondary hyperaldosteron....more sodiun retension....so Hypervolemic hypernatremia....
Though liver metabolizes aldosterone more slowly than it used to it is the reduced blood flow to the kidney that causes the hypoaldosterinism.. Reference Harrison's 17th edition
 

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but wt about blood pressure...??
if there is hypernatremia n hypervolumia...sholdn't it rise...!!
hmm.....may be the fluid that the body is retaining is contributing to ascitic fluid only...n not to intravascular compartment...
so again going in favour of C Hypervolemic hypernatremia....
waiting for correct ans...:eek:
 

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hmm ...I would stick with

B. Hypovlemic Hypernatremia

If we review the options....

A. Excessive insensible losses, primarily of water (euvolemic hypernatremia)

It cannot be inc. insensible losses, there is no mention/hint of any condition which can lead to inc. sensible loses. So it can't be A.

C. Hypervolemic hypernatremia

Pt's HR is 110/min & its specifically mentioned that he has absent peripheral edema. All pointing towards hypovolemia. So it rules out hypervolemia.

D & E options are both similar so we are left with option B.

I hope i am right....
 
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Discussion Starter · #18 ·
ANSWER+EXPLANATION (From MedicalExams.com)

Wow. Great discussion guys.

The correct answer is Choice B.

There are a number of key points to take on board:
1. hypernatremia is a disorder of water balance, most often a water deficit
2. sodium is an effective osmole, so hypernatremia = hyperosmolality
3. hyperosmolality leads to cellular dehydration, most often in the brain, and this is serious
4. the speed with which hypernatremia occurs determines the symptomatology and the required rate of collection
5. hypernatremia is associated with a higher risk of death in most patient groups

Hypernatremia can occur through loss of water alone without any deficit in sodium (pure water loss) or can occur in a setting
where sodium and other electrolytes are also lost with water, but the fluid is hypotonic and the water loss greater than the
electrolyte loss. These two mechanisms are the commonest contributors to hypernatremia. It is possible to develop hypernatremia
through administration of excessive sodium e.g. hypertonic saline or bicarbonate, but this is not common.

Our patient in this case has been taking lactulose as part of the management of his cirrhosis and encephalopathy, and his case
raises a number of issues relating to the genesis and maintenance of his hypernatremia.

1. lactulose causes an osmotic diarrhea in which water is lost in excess of electrolytes (hypotonic fluid losses)
2. encephalopathy can impair our primary defense against hypernatremia, which is thirst and water ingestion. Elderly,
debilitated, or encephalopathic patients are at particular risk
3. secondary hyperaldosteronism in severe cirrhosis creates a tendency to sodium retention and potassium loss
4. significant hypokalemia such as this man has may impair renal concentrating mechanisms preventing proper defense
against hypovolemia

Our patient has clinical evidence of hypovolemia, and nothing to suggest excessive insensitive losses. As the hypernatremia
progresses it may worsen the patients CNS status and even further diminish his chances of self-correcting....so it is up to his
doctor to recognize and correct this abnormality.

At this point you need to be able to work out:
1. the size of the water deficit that you need to correct
2. the time over which you will correct it
3. what effect the administration of different crystalloids will have on serum sodium

There isn't space here to go into that in depth, so please review the references. However, there are three equations that you will
need to keep in mind.

First of all, let's calculate the water deficit:
Water deficit to correct hypernatremia = total body water (TBW, in litres) x [(actual sodium/desired sodium)-1]
and where TBW = 0.6 x lean body weight for men and 0.5 x lean body weight for women.

and where TBW = 0.6 x lean body weight for men and 0.5 x lean body weight for women.
e.g. Male with LBW 70kg, Na+ 162: deficit = 0.6 x 70 x [(162/140)-1] = 42 x (1.16 - 1) = 6.7 Litres deficit

Secondly, how quickly should it be corrected?

In general, symptomatic patients who have developed their hypernatremia rapidly over less than 48 hours should initially have
their sodium reduced by 1-1.5 mmol/L/hour until the sodium is around 150 mmol/L or their symptoms improve. To calculate the
deficit to replace to get down to 150 mmol/L you can insert it into the equation above. If your patient developed hypernatremia
more slowly, then correction should proceed at the slower rate of 0.5 mmol/L/hour because there may have been some osmotic
equilibration in the meantime which places them at greater risk of cerebral edema from over-rapid correction, and this can have
serious consequences including patient death. The equations and suggestions given here do not constitute medical advice and are
for educational purposes only.

Lastly, what are the effects of different fluids on plasma sodium?

This can be calculated from the equations below.
Change in serum Na+ from 1L of infusate = (infusate Na+ - serum Na+)/(TBW +1).
If you fluid contains sodium and potassium then this alters the equation and the volume required to correct the deficit. The
equation becomes:
Change in serum Na+ from 1L of infusate = (infusate Na+ + infusate K+ - serum Na+)/(TBW+1)
Obviously the lower the electrolyte concentration infused the greater the reduction in serum Na+.

Suggested References
Adrogue HJ, Madias NE. Hypernatremia. NEJM 2000; 342: 1493-1499.
Liamis G, Haralampos HJ, Elisaf M. A review of drug-induced hypernatremia. NDT Plus 2009; 2: 339-346.
 
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