Practice MCCEE/MCCQE question 1- tough!

[medistudent]

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)

 

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

 

Answer before looking at the explanation....

 

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Explanation (courtesy of the new LMCCexams.com - they have 1800 new questions made by our Canadian professors)

 

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.

 

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+.

 

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[MarkSeve808]

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