NR 507 Week 2 SIADH Pathophysiology Case Analysis Example

A Sodium of 121 in a Retired Roofer, 71, With a New Lung Mass: Explaining His Confusion, His Concentrated Urine and His Normal Exam From Ectopic Antidiuretic Hormone Upward

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College of Nursing, Chamberlain University

NR 507: Advanced Pathophysiology

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Month Day, Year

A Sodium of 121 in a Retired Roofer, 71, With a New Lung Mass: Explaining His Confusion, His Concentrated Urine and His Normal Exam From Ectopic Antidiuretic Hormone Upward

What the Patient Presents With

Mr. T., 71, a retired roofer who smoked a pack a day for 45 years, was brought in by his daughter after three days of nausea, poor appetite and increasing confusion. Two weeks earlier, a chest radiograph for a persistent cough had shown a right hilar mass, and he was awaiting bronchoscopy. On arrival he was oriented to person only, with no focal neurologic deficit. Blood pressure was 134/78 mm Hg without orthostatic change, heart rate 82, and he had moist mucous membranes, no edema, no jugular venous distension and normal skin turgor.

His laboratory values were: serum sodium 121 mmol/L, potassium 4.1 mmol/L, glucose 96 mg/dL, blood urea nitrogen 8 mg/dL, creatinine 0.7 mg/dL, uric acid 2.6 mg/dL and measured serum osmolality 252 mOsm/kg. Urine osmolality was 520 mOsm/kg and urine sodium 58 mmol/L. Thyroid-stimulating hormone and a morning cortisol were normal. This paper explains why this man, with this history, presents in this particular way, and it gives every abnormal value a reason and every relevant normal value a job.

The Fault at the Bottom

The underlying fault is almost certainly production of antidiuretic hormone (ADH) by the tumor itself. Small cell lung cancer, the tumor most strongly linked to heavy smoking and a central, hilar location, arises from cells with neuroendocrine properties, and some of these tumors synthesize and secrete ADH regardless of the body's osmolality or volume. That secretion is "inappropriate" in the precise sense: it continues when the plasma is already dilute, which normally switches ADH off almost completely (Ellison & Berl, 2007). Bronchoscopy is still pending, so the tumor type is a working inference, but the presentation fits it closely.

From Fault to Finding

Concentrated urine in dilute blood. ADH binds V2 receptors on the principal cells of the renal collecting duct and causes aquaporin-2 water channels to be inserted into the luminal membrane. Water then moves out of the tubule into the hypertonic medulla, and the urine is concentrated. In a person with a serum osmolality of 252 mOsm/kg, the kidney should be excreting the most dilute urine it can, below 100 mOsm/kg. Mr. T.'s urine was 520 mOsm/kg. That single pairing, dilute blood and concentrated urine, is the clearest evidence in the case that ADH is acting when it should not be.

Low sodium. The sodium has not been lost; it has been diluted. The water retained under ADH's influence, combined with ongoing intake, expands total body water, and sodium concentration falls. This is why the measured osmolality is low, 252 mOsm/kg, and why the calculated value, about 250 mOsm/kg from twice the sodium plus the glucose and urea contributions, agrees with it.

Urine sodium of 58. A patient who was losing sodium and water together, through vomiting or diarrhea, would be conserving sodium, with a urine sodium below about 30 mmol/L. Mr. T. is excreting sodium freely. The retained water expands his circulating volume slightly, and the body responds with natriuresis: pressure natriuresis and natriuretic peptides increase sodium excretion. The kidney is behaving correctly for a slightly volume-expanded state, which is exactly what SIADH produces.

Low urea nitrogen and uric acid. A BUN of 8 mg/dL and a uric acid of 2.6 mg/dL are low. Mild volume expansion increases their renal clearance, and a low uric acid in a patient with hyponatremia is a recognized supporting clue for SIADH rather than volume depletion (Ellison & Berl, 2007).

Confusion and nausea. The brain is where the dilution becomes dangerous. When plasma osmolality falls, water moves down its concentration gradient into brain cells, which swell inside a rigid skull. Neurons respond over roughly two days by exporting potassium, sodium and organic osmolytes to reduce their water content, which limits the swelling. Mr. T.'s symptoms developed over three days, suggesting that the fall was gradual enough for partial adaptation, which is why he is confused rather than seizing. That same adaptation is the reason his sodium must be corrected slowly: a brain that has shed its osmolytes cannot regain them quickly, and a rapid rise in sodium can shrink cells and damage myelin in the pons and elsewhere (Spasovski et al., 2014).

The Normals That Do Work

Several normal findings are as important as the abnormal ones, because each rules out a rival explanation.

The normal glucose of 96 mg/dL rules out hyperglycemia pulling water out of cells and diluting the sodium, a translocational hyponatremia that would come with a normal or high osmolality.

The normal volume examination, with no orthostasis, no edema, no jugular distension and moist mucous membranes, rules out the two other large groups of hyponatremia: volume depletion, where ADH is appropriately released in response to low volume, and edematous states such as heart failure or cirrhosis, where ADH is released because the circulation is perceived as underfilled.

The normal TSH and morning cortisol exclude hypothyroidism and adrenal insufficiency, both of which can cause a hyponatremia that mimics SIADH and must be ruled out before the diagnosis can be made (Spasovski et al., 2014).

The normal potassium and creatinine argue against diuretic effect and kidney failure, and his medication list, which his daughter brought, contained no thiazide or other drug commonly linked to hyponatremia.

The Conclusion as a Consequence

Taken together, the findings lead to a single explanation that accounts for all of them: a clinically euvolemic, hypo-osmolar hyponatremia with inappropriately concentrated urine and high urine sodium, with thyroid and adrenal causes excluded, in a heavy smoker with a central lung mass. That is the syndrome of inappropriate antidiuresis, most likely from ectopic ADH produced by a small cell carcinoma. The diagnosis follows from the chain of findings; it was not attached to them afterward.

The explanation also predicts what should happen next. Fluid restriction should raise his sodium slowly, because it limits the free water his kidneys cannot excrete. Isotonic saline alone may worsen it, because his kidneys will excrete the sodium in concentrated urine and keep much of the water. And if the tumor responds to chemotherapy, the sodium should improve as the source of ADH shrinks, which would be the final confirmation of the mechanism.

References

Ellison, D. H., & Berl, T. (2007). The syndrome of inappropriate antidiuresis. New England Journal of Medicine, 356(20), 2064-2072. https://doi.org/10.1056/NEJMcp066837

Spasovski, G., Vanholder, R., Allolio, B., Annane, D., Ball, S., Bichet, D., Decaux, G., Fenske, W., Hoorn, E. J., Ichai, C., Joannidis, M., Soupart, A., Zietse, R., Haller, M., van der Veer, S., Van Biesen, W., & Nagler, E. (2014). Clinical practice guideline on diagnosis and treatment of hyponatraemia. European Journal of Endocrinology, 170(3), G1-G47. https://doi.org/10.1530/EJE-13-1020