A 57-year-old unconscious man was brought to the hospital having had generalized seizures one hour earlier. His wife stated that he had been feeling tired for several months, during which time his appetite had declined and he had lost 20 pounds. His long-standing cough had become gradually more severe and he had coughed up bright red blood twice during the past 2 weeks. He had smoked heavily for over 25 years.

Physical Examination Weight 80 kg, BP 145/90, pulse 120, Temperature 99.6o F, R 28. He was a comatose, somewhat wasted looking male. There was no edema. Fingernails were clubbed. Neurological exam showed slightly overactive but symmetrical reflexes. There was dullness, and diminished breath sounds over the right lower lung field posteriorly. Heart size and sounds were normal.

 Chest x-ray: Pleural effusion and hilar enlargement on the right.

1. Calculate serum osmolarity and compare to measured value. What does this tell you?

Review: measured vs calculated osms

 
Osm = (2 x Na) + Gluc/18 + BUN/2.8 = 229 (same as measured)

When meas osms are > calc osms by at least 10 mosm/kg, an OSMALAL GAP exists, and suggests the ingestion of a substance with osmotic activity

No osmolal gap, therefore no exogenous oms present (EtOH, mannitol)

 

2. Under what circumstances can the serum Na concentration be low despite normal salt and water balance?  Would measured and calculated serum osmolality be abnormal in these circumstances?

Presence of a non-sodium substance in the serum that has physiologic osmolal activity: glucose, mannitol

nb. I have dropped pseudohyponatremia from the discussion, as modern autoanalyzers are not affected by serum lipids/proteins.

Go over measured osms as a physical test of osms, sim. to freezing pt. depression-does NOT necessarily equal a physiologic osmotic effect.

Discuss mechanism of:

 
a. hyperglycemia: meas osms ­ , calc osms ­ , serum Na ¯

 b. mannitol: meas. osms ­ , calc osms ¯ , serum Na ¯

 c. hyperlipidemia, paraproteinemia: meas osms normal, calc osms ¯ , serum Na ¯

  d. uremia: meas osms ­ , calc osms ­ , serum Na normal

 

The ability to lower serum Na is a measure of the substances effictive osmolality across cell membranes.


 
 

3. How is total body water changed from normal in this patient?  Extracellular volume?   Explain this discrepancy.

TBW elevated. ECV normal (by clinical exam)


An initial increse in TBW and ECV leads to Na excretion by the kidney (note UNa >30), normalizing ECV, but still with high TBW and a very high intracellular volume. With normal salt intake, a new steady state is reached in which sodium excretion balances dietary intake. So UNa is not <10 (comp. CHF, cirrhosis)

 
 

4. What is the likely mechanism of this patient's severe hyponatremia?   What are other causes of euvolemic hyponatremia?

 

SIADH 2° lung Ca (also nausea, psychosis, pancreatic Ca, other pulmonary disorders, CNS trauma or tumor).

 

· euvolemic hyponatremia also can be 2° to:

-diuretics (esp. HCTZ), psychiatric drugs, psychogenic polydipsia, hypothyroidism, glucocorticoid deficiency

 

5. What would urine osmolality be in a patient with normal water regulation whose serum Na was lowered to 120? Why is urine not more dilute in this patient?

 Normal person: Uosm would be 50 mosm/kg: ADH turned off. Point out that normal range of Uosm= 50-1200 mosm/kg.

 Patient: Unregulated ­ in ADH causes ­ collecting duct permeability and water reabsorption.

 

6. Predict the effect of administering 1 liter of 0.9% normal saline to this patient. What is best immediate treatment for the hyponatremia? Best longterm treatment?

                The hyponatremia would worsen. Sodium would be excreted, while water was retained. To make progress, the administered fluid must be MORE CONCENTRATED THAN THE PATIENT'S URINE (here, Uosm = 480).